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Vanessa T. Kline, PharmD, BCPS

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Although the presence of Birbeck granules is considered the gold standard for identifying Langerhans cells ultrastructurally virus software order zyvox now, few laboratories employ electron microscopy in diagnostic pathology in the modern era virus and trip discount zyvox amex, relying instead on the phenotypic analogue of the Birbeck granule, namely, langerin expression detected immunohistochemically. Langerin is localized in the Birbeck granules, organelles present in the cytoplasm of Langerhans cells that manifest a zippered membrane. It is a C-type lectin with mannose-binding specificity, and it has been proposed that mannose binding by this protein leads to internalization of antigen into Birbeck granules and provides access to a nonclassical antigen-processing pathway. In one series, Birbeck granules and langerin expression were only observed in a minority of cutaneous Langerhans cell sarcoma cases (Ben-Ezra et al. Differential diagnosis the differential diagnosis of Langerhans cell sarcoma includes anaplastic large cell lymphoma, histiocytic sarcoma, dendritic cell sarcoma, myeloid dendritic cell leukemia, blastic plasmacytoid dendritic cell tumor, and monoblastic leukemia cutis. There may be Cutaneous Infiltrates of Myeloid Derivation 513 considerable histologic overlap and therefore immunohistochemistry is critical to this distinction. The phenotypic profile supported their classification as being of one of myeloid dendritic cell origin. The eruption was papulonodular in nature, the lesions tended to follow a course of spontaneous regression and there was a strong association with an underlying hematologic disorder; all patients had a biopsy-proven chronic myeloproliferative disease, either myelodysplastic syndrome, chronic myelomonocytic leukemia, or myelofibrosis in eight of the nine cases. In some patients with chronic myeloproliferative disease, the development of this form of skin eruption could be a harbinger of a more aggressive clinical course, with transformation into acute leukemia. Keratinocytes, which populate the hair follicle, express the appropriate chemokine receptors that lead to the migration of precursor monocytic cells to the hair follicle, especially triggered by trauma (Nagao et al. Such cells may play a role in launching an antiviral response and have also been identified in the setting of systemic lupus erythematosus. Eight patients in our series had a prior or subsequent diagnosis of a myeloproliferative disorder representing chronic myelomonocytic leukemia in four cases, myelofibrosis in two cases and advanced myelodysplastic syndrome in two cases. It seems likely that the neoplastic myeloid dendritic cell likely arose from the same neoplastic clone implicated in their underlying myeloproliferative disorder. In our patients, the eruption was associated with an accelerated clinical course and or worsening symptoms in at least six of the nine cases, suggesting that the cutaneous infiltrate was a harbinger of either disease progression or conversion to acute myeloid leukemia. It seems likely that monocytosis in the context of chronic myeloproliferative disease is prognostically significant; in one study, primary myelofibrosis complicated by monocytosis was uncommon, being identified in only 10 of 237 cases of primary myelofibrosis during the course of the disease (Boiocchi et al. The patients could exhibit a shift from primary myelofibrosis to overt chronic myelomonocytic leukemia and/or an increase in circulating blasts. Vitte and coworkers reported 16 cases with cutaneous infiltrates of what they termed mature plasmacytoid dendritic cell proliferations, which presented mostly as papules and nodules, many in patients that had chronic myelomonocytic leukemia or acute myeloid leukemia (Vitte et al. The main cytogenetic abnormality uncovered in the paraffin-embedded Light microscopic findings the histologic findings are those of a wel-differentiated monocytic infiltrate, namely a diffuse pattern of dermal infiltration with superficial accentuation, or an organized, noneffacing nodular perivascular and periadnexal dermal pattern, as described in the vignettes. The distinction cytomorphologically from a leukemic monoblast includes a smaller cell size, a relatively low nuclear to cytoplasmic ratio, a greater extent of cytoplasm, and a lack of pleomorphism. In many instances the lesions exhibit spontaneous regression; however, they can attain a very large size and become life-threatening (Stover et al. The more common sites of involvement are the skin, gastrointestinal tract, brain, kidney, liver, and lung. A growing number of cases are reported that primarily and/or exclusively involve the skin. We have encountered patients with clonally restricted plasma cell infiltrates and, in a number of cases, a prominence of IgG4 positive plasma cells. In this regard one might view the histiocytes as innocent bystanders secondary to the cytokine milieu associated with the polytypic or light chain restricted plasma cell infiltrate. Light microscopic findings Light microscopic findings Histologically, the histiocytes are large, with voluminous cytoplasm of grey to lightly eosinophilic-staining quality. The cells are characteristically mononuclear, but exhibit emperipolesis of engulfed cells surrounded by cytoplasmic halos. Subcutaneous extension may be prominent, defining a lymphomatoid and granulomatous histiocytic lobular panniculitis. The diagnosis can be difficult to make because of the degree of background lymphocytic and plasma cell infiltration and the deep, effacing infiltrates can mimic panniculitis-like T cell lymphoma. The biopsies show a nonepidermotropic histiocytoid infiltrate that spans the full thickness of the dermis, with a variable admixture of eosinophils, neutrophils, and lymphocytes. As with other forms of dermal dendritic cell histiocytopathy a certain degree of pleomorphism can be seen. Where the atypia is particularly striking we have seen cases misinterpreted as atypical Spitz tumors. It is important to remember that a histiocyte of the dendritic cell type can undergo transdifferentiation to other dendritic cells. Other organ systems can be involved, such as the lymph nodes, spleen, and bone marrow. The main mucosal sites involved are the trachea and larynx, resulting in symptoms of hoarseness and dyspnea. Posterior fossa involvement is associated with mortality in most cases; bone involvement is rare. There may be spontaneous resolution, although infiltration of certain critical structures, such as the trachea and pituitary gland, can have significant adverse sequela. Phenotypic studies the cells are of monocytic lineage and hence terminally differentiated monocytic markers are positive. The classic symptoms are those of massive bilateral cervical lymphadenopathy accompanied by fever, elevated erythrocyte sedimentation rate, anemia, and polyclonal hypergammaglobulinemia. Although the etiologic basis is unclear, there is an association with underlying autoimmune disease and hematologic dyscrasias. It has been postulated that a viral stimulus could be pathogenetically significant and/or that an aberrant histiocytic response to antigen could be operational. Roughly half of cases show involvement of a lymph Light microscopic findings the biopsies characteristically show a sheet-like proliferation of markedly lipidized cells. There have been a few cases described in children; less than 50 cases have been reported worldwide. The onset of this disease in adults is typically in the third to sixth decades of life, while in children, the commencement is before the age of four. The papules usually have a striking symmetrical disposition and rarely involve mucosal surfaces or viscera. Within several months, the lesions resolve, leaving behind hyperpigmented macules (Lan et al. The etiology of the condition is unknown, but likely reflects a clonal disorder of myelomonocytic cells. It is unclear if the eruptions have the same association with underlying myeloproliferative disease as conditions such as histiocytosis X (Klemke et al. This condition is considered an aggressive form of histiocytopathy due to a high incidence of lung and cardiac involvement. Skin involvement can occur, but not as often as the long bones of the axial skeleton, the orbit, the central nervous system, heart, and lung. The involvement of the lung is characterized by progressive restrictive lung disease reflective of pleural infiltration by histiocytes accompanied by a peculiar pattern of hyalinizing fibrosis (personal observations). Light microscopic findings Light microscopic findings Biopsies typically show an extensive dermal histiocytic infiltrate, accompanied by dermal mucin deposition. The histiocytes are notable for their voluminous, basophilic cytoplasm, apparently containing mucin. In addition, the presence of other inflammatory cell elements, including plasma cells and neutrophils, is also an intrinsic feature of these diseases (Perrin et al. In point of fact, there is considerable clinical and histopathologic overlap between these entities. However, the primarily monotypic histiocytic infiltrate, the immunohistochemical profile, the lack of Langerhans cell marker expression, the absence of xanthomatous cells, and the clinical presentation including the regression of the lesions rule out the other differential diagnoses (Sagransky et al.

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The diagnosis can and should wait until it can be made with confidence; no screening tests are ever indicated virus 4 year old cheap zyvox 600mg on line. If the patient has a clinical picture compatible with the disease infection in the blood cheap zyvox 600 mg, the evaluation should progress to the most appropriate and powerful laboratory test available. Using my example of Cushing syndrome, the only reliable test that can be ordered is the 24-hour urinary free cortisol excretion. Measurement of the cortisol production rate using tritiated or deuterated cortisol infused to a constant plasma concentration is even better and the only test possible in patients with renal failure. Because cortisol has a diurnal secretory pattern, even when caused by an adrenal adenoma, only a test that can integrate plasma free cortisol over a 24-hour period is useful. No signs Physical Examination In addition to an examination focused on the findings of the endocrine disease, the essential physical examination expected of a competent internist is required. A careful examination of the heart, lungs, abdomen, and neurologic systems is expected by the patient and the referring physician. As William Osler famously said, "It is the responsibility of the consultant to do the rectal examination. The general opinion of most referring physicians is that endocrinologists are also complete internists. I often find that I am the only doctor who has carefully listened to the heart, percussed the lungs, and examined the external genitalia. I am often the first doctor to diagnose Parkinson disease in a referred patient and virtually always the first to diagnose clinical depression or early dementia. Mastering the physical examination will dramatically enhance your ability to define and manage the endocrine diseases you diagnose. This chart illustrates the interplay between the clinical presentation and the laboratory test for the disease. Deciding when to make the call is an example of the art of medicine (inductive logic). High urinary free cortisol and classic clinical features define Cushing syndrome as first described. On occasion, a high urinary free cortisol will be found in a person with no signs of Cushing syndrome. The elevated levels of urinary free cortisol unaccompanied by classic clinical signs of Cushing syndrome occur in two settings. The development of the classic signs of Cushing syndrome are almost always associated with weight gain. If weight gain is prevented, as by the anorexia associated with an occult malignancy, the classic signs of Cushing syndrome cannot appear, but the mineralocorticoid action of cortisol will be fully expressed. If any of these tests is applied to a person who does not have glucocorticoid excess, the diagnosis of Cushing disease will be made. The treatments that follow are futile and, in the worst case, will result in an otherwise normal person who has no pituitary or adrenal glands. It is the result of too many tests and a deficient understanding of the pathophysiology of the disease. The dexamethasone suppression test was developed by Grant Liddle and his group at Vanderbilt in 1960. The normal basal excretion of 17-hydroxycorticoids ranged between 3 and 12 mg/day. Applying the test to a group of 27 patients who had Cushing syndrome showed that none of them suppressed urinary 17-hydroxycorticoids to less than 3 mg/day. On the basis of these data, they concluded that suppression of urinary 17-hydroxycorticoid to less than 3 mg/day excludes Cushing syndrome caused by a pituitary microadenoma or an adrenal tumor, the only causes of Cushing syndrome known at the time. The corollary to this conclusion, that the failure to suppress 17-hydroxyglucocorticoids to less than 3 mg/day with dexamethasone is diagnostic of Cushing syndrome, however, is not true. We now know that there are many situations in which dexamethasone at 2 mg/day will not suppress cortisol secretion. Such situations include obesity, physical and mental stress, depression, and psychosis. Nine percent of these people, at any given time, have clinical depression: 10 million people. Of these, conservatively 50% will fail to suppress plasma cortisol following dexamethasone: 5 million people. The prevalence of noniatrogenic Cushing syndrome is 5 to 10 cases per 1 million people; let us say, 5000 people. Assume that all of these people fail to suppress plasma cortisol after an oral dose of dexamethasone. Thirty percent are obese (5 million people), and 10% are depressed (500,000 people). Assume that all people with Cushing syndrome began as an incidental adenoma, and it requires 3 years to be large enough to detect. The dexamethasone test has only a single remaining venue: dexamethasone suppressible hypertension. It needs to go the way of the protein-bound iodine, 17-ketosteroids, and the rabbit test for pregnancy. A Digression into Test Technology Endocrinologists love ordering and interpreting tests. In order for the tests to be helpful, however, several performance characteristics must be known. This algorithm illustrates the sequential application of the tests of differential diagnosis. This is a good example of the application of the experimental method in medicine (deductive logic). Plasma cortisol can never be used to diagnose adrenal insufficiency, yet it is commonly employed in this way. Second is the coefficient of variation (the standard deviation in percent) of the test. This number should be as low as possible in the range of the test we are most interested in. If the coefficient of variation is 5%, then numbers falling between 40 mg/dL and 60 mg/dL are not different from each other with 95% confidence. This "sweet spot" can be moved up or down by increasing or decreasing the antibody concentration. Sometimes the laboratory will respond to your need for a given value to be as precise as possible, but not often. Nonetheless, the endocrinologist should be able to know when two values are different from each other. The guidelines are these: always replace a hormone deficiency with the hormone that is missing. All of the other hormones have been modified, usually to enable oral administration. Cortisol, as an example, has a tightly regulated metabolic clearance rate with a half-life of 80 minutes. The half-life of dexamethasone varies between 60 and 360 minutes, making it virtually impossible to find the appropriate replacement dose. Half of our daily mineralocorticoid effect comes from cortisol, another reason to use the natural hormone. Patients on the ideal replacement regimen will still have good days and bad days, just like anyone. They will attribute their bad days to improper replacement and often try to change the plan. If you do, the patient will attribute any unpleasantness to the change, which is, of course, a non sequitur. The gifted endocrine surgeons are scattered across the country, but all can be reached.

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We would tend to favor the view that several of these cases in adolescent children represented this entity antibiotics for acne in pakistan order zyvox with american express. The histopathology presented in this paper is virtually identical to what we presented in our paper antibiotic resistance of helicobacter pylori in u.s. veterans cheap zyvox 600 mg mastercard, including the lack of large cell trasnformation and striking follicular hyperkeratosis. It is well established that conversion from a Th1-dominant microenvironment to one associated with a Th2 profile correlates with a more aggressive clinical course. The local cutaneous cytokine milieu recapitulates the acute vesicular phase of an eczematous process (McBride et al. It is a distinctive variant of granulomatous mycosis fungoides, as will be discussed presently. The authors documented extracutaneous spread in 26% of patients with secondary lymphoid neoplasms developing in 21%; one-third of patients died from their disease, typically reflective of tumor progression (Kempf et al. A very curious finding was the identification in all patients of intrapulmonary granulomatosis, which was not in the context of representing granulomatous mycosis fungoides involving the lung, but potentially suggestive of the type of sterile granulomatous inflammation observed in patients with underlying immunodeficiency. The diagnosis of granulomatous slack skin is made based on an integration of characteristic clinical features with distinctive light microscopic findings, which are alluded to below. In this variant, the patients develop large areas of loose skin with a predilection to involve intertriginous areas and other regions of the body with relatively redundant skin. A point of reiteration is the similarity of this condition clinically and light microscopically to the interstitial granulomatous drug reaction. While interstitial infiltration is characteristic of the interstitial granulomatous drug reaction, significant elastolysis characteristic of the granulomatous slack skin does not occur (Li et al. Interstitial mycosis fungoides There are two broad categories of mycosis fungoides accompanied by a significant histiocytic infiltrate namely granulomatous mycosis fungoides and interstitial mycosis fungoides, with both representing a morphologic continuum of a distant form of mycosis fungoides. The patient presented with infiltrative plaques temporally associated with calcium-channel blocker therapy. However, over the ensuing months her skin rash became very extensive with progressive hardening of the skin despite drug cessation; 1 year after discontinuing her drug she continues with progressive disease. A diagnosis was made of granulomatous mycosis fungoides possibly arising in a background of the interstitial granulomatous drug reaction. An important clue to the diagnosis is the basilar colonization unaccompanied by destructive epithelial changes and the narrow grenz zone separating this subtle intraepidermal component from the overlying epidermis. Higher-power magnification shows cer- ebriform lymphocytes colonizing the epidermis. In the latter, the lesions have a diffuse interstitial infiltrate of histiocytes which is typically less than 30% of the infiltrate. There is significant clinical, histologic, phenotypic and molecular overlap with the interstitial granulomatous drug reaction in which there may not be an obvious temporal association between the onset of lesions and the initiation of therapy with the implicated drug. Like mycosis fungoides, the lesions are large and indurated, manifesting a close clinical resemblance to granulomatous and plaque-stage mycosis fungoides and with a distribution reminiscent of that seen in granulomatous slack skin. Commonly implicated drugs include statins, angiotensin- converting enzyme inhibitors and calciumchannel blockers (Magro et al. In some cases the syndrome appears in a patient with a stable form of patch- or plaque-stage mycosis fungoides, while in other cases the disease appears de novo or arises in a background of idiopathic erythroderma associated with severe pruritus, scaling, lichenification, alopecia, and nail dystrophy. In this variant the palms are hyperkeratotic and oftentimes fissured and there may be an ectropion. Significant zones of superficial colloid body formation are noted, compatible with a lichenoid tissue reaction. At variance with lichen planus is the degree of cytologic atypia and significant areas with passive migration of lymphocytes into the epidermis. We and others feel that the emergence of T cell clonality, while a feature that suggests a lymphoid dyscrasia, should not be equated with malignancy. In the setting of atopic eczema the dysregulated cell populace is reactive, while in erythrodermic cutaneous T cell lymphoma, the cells are neoplastic. In all three conditions there can be peripheral blood eosinophilia and high IgE levels as a sequelae of elevated levels of interleukin 5, a Th2 product. In addition the serum lactate dehydrogenase and interleukin 2 receptor are elevated in all three disorders. If the patient has a longstanding history of atopy with documented allergies to various antigens then erythrodermic eczema is more likely to be the diagnosis. The radioallergicsorbent assay is positive in the setting of atopic eczema in virtually all cases. Conversely, in erythrodermic eczema the lymphocytes can appear atypical and infiltrate the epidermis, especially if an antigenic trigger was the precipitating factor to eventuate into an erythrodermic state. These observations are in direct contrast to those by Abel and coworkers, where they reported an association between the atopic diathesis and the development of both leukemic and nonleukemic erythrodermic T cell lymphoma (Abel et al. We have seen a few cases of patients, characteristically in their fourth or fifth decades of life with longstanding severe atopic dermatitis developing erythrodermic cutaneous T cell lymphoma. Important differentiating features clinically include striking facial edema, hepatomegaly, and fever. The skin biopsies can resemble mycosis fungoides by virtue of the presence of cerebriform atypia, epidermotropism, follicular mucinosis, phenotypic abnormalities and clonality. Differentiating light microscopic features include significant spongiosis, necrotic keratinocytes, a dominant perivascular distribution of the dermal infiltrate with many transformed perivascular cells. However, we have seen cases of erythrodermic mycosis fungoides where the process likely arose in a background of a drug-associated lymphomatoid hypersensitivity reaction or longstanding atopy where features such as vesiculation and spongiosis may be conspicuous. The epidermis typically shows an irregular pattern of epidermal hyperplasia with parakeratosis. There is greater heterogeneity with respect to the phenotypic profile in lesions of mycosis fungoides. Prognosis the most important predictor of survival is the extent of clinical disease, as defined by the stage Table 12. Early cutaneous disease (Stage I) is divided into Stage I T1 when less than 10% of the entire body surface is involved versus Stage I T2 when more than 10% of the body surface is affected. Early-stage mycosis fungoides may progress to T3 and T4 with the advent of tumor development and erythrodermic mycosis fungoides, respectively. Patients with limited disease have a 5-year survival no different from the general population, while those patients with more advanced disease, especially in the context of extracutaneous dissemination, have a more ominous prognosis. In one study a total of 4892 patients with mycosis fungoides were identified, where the median follow-up was approximately 58 months. The utilization of radiation treatment was less likely in females than males although it was more likely to be utilized with advanced age and higher stage. A comprehensive study regarding prognosis and treatment was performed by the Dutch lymphoma group. At the time of presentation, over 90% of patients with mycosis fungoides initially had skin disease only and less than 10% presented with concurrent nodal or visceral involvement. An important predictor of enhanced survival was entry into complete remission following initial treatment.

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Syndromes

  • Radiation therapy
  • Thyroid scan and uptake
  • Trauma
  • The newborn  is placed under the lights without clothes or just wearing a diaper.
  • Age
  • Fistula (abnormal passage) between the vagina and the skin
  • Personal worry
  • Benztropine (Cogentin)

Waardenburg syndrome, type 4

However virus 51 purchase online zyvox, radiologists should be aware of the fact that utilization of low tube current or low peak kilovoltage (kVp) results in increased image noise ucarcide 42 antimicrobial buy cheap zyvox online. Additional advantages of image-guided biopsy include the ability to be performed on many individuals as outpatients, a comparatively smaller amount of time in recovery, and the ability to evaluate the lungs and the remainder of the chest for complications during and after the procedure. However, in current clinical practice, core needle biopsy specimens are preferred as a greater volume of intact tissue can be obtained. This is especially important given the greater volume of tissue needed for detailed analysis, such as genetic and biomarker testing. However, there is currently no definitive data regarding optimal guidelines for imaging follow-up of patients after treatment. Following curative intent therapy (surgical resection, chemotherapy, &/or radiation therapy), there are two specific objectives: the detection of recurrent lung cancer and new primary lung cancer. National Lung Screening Trial Research Team et al: the National Lung Screening Trial: overview and study design. In this high-risk patient with emphysema, the nodule is concerning for malignancy. Failure to respond to medical therapy raised concern for multifocal adenocarcinoma or lymphoma. The estimated error rate for detecting early lung cancer on radiography is 20-50%. Abnormalities in specific locations, such as the lung apices, paramediastinal, hilar, and retrocardiac lung zones and lung bases, may be difficult to visualize on radiography. Bone suppression techniques and other aids can be used to improve accuracy of radiographic interpretation. This lesion was suspicious for lung cancer and biopsy confirmed primary pulmonary carcinoma. Most lung cancers recur in the first 5 years following therapy, peaking at years 2-3. Fungal infection may mimic lung cancer when it manifests with masses and lymphadenopathy. Note posterior displacement of the major fissure and bronchovascular structures forming the characteristic "comet tail" sign. Demonstration of intrinsic fat attenuation within the lesion is a characteristic imaging feature of lipoid pneumonia. The endobronchial tumor is the smaller component of the iceberg growth pattern characteristic of central airway carcinoids. The imaging features of pneumonia may closely mimic those of invasive mucinous adenocarcinoma. Note the small left upper lobe nodule, which is visible on radiography in retrospect. The presence of an obvious abnormality may cause radiologists to neglect other subtle findings, known as the satisfaction of search phenomenon. Various bone suppression techniques have been shown to improve sensitivity for detection of lung nodules. Lung cancer manifesting as bullae and cystic lesions with thickened walls are known causes of missed lung cancer. Although this nodule can be characterized as category 3, the presence of spiculation allows upgrading to category 4X. Biopsy of nodules in this location is challenging due to significant respiratory motion. Right side down positioning optimized the biopsy approach by nearly eliminating respiratory motion. Huang K et al: Follow-up of patients after stereotactic radiation for lung cancer: a primer for the nonradiation oncologist. New soft tissue and convexity of previously radiated area and filling in of bronchiectatic airways are consistent with recurrent disease. These include malignant neuroendocrine carcinomas, such as typical and atypical carcinoid tumors, sarcomas, such as primary pulmonary synovial sarcoma and Kaposi sarcoma, and benign lesions, such as hamartoma. Associated findings, such as a pleural effusion, representing chronic acute or recurrent hemothorax, may be present. However, in many cases, pulmonary findings such as nodules, masses, or consolidations, are nonspecific and require histologic sampling for definitive diagnosis. Nodules are typically peribronchovascular in distribution and tend to coalesce into larger opacities. Other findings, such as peribronchovascular and interlobular septal thickening and fissural nodularity, have been described. In this introductory chapter, we will consider typical and atypical carcinoid tumors. Carcinoid Tumor Carcinoid tumors are neuroendocrine neoplasms typically found in the gastrointestinal tract; however, 20-30% of all lesions arise from the respiratory tract and comprise 1-2% of all primary lung cancers. Carcinoid tumors are classified based on mitotic activity: Typical (low grade) and atypical (intermediate grade). Atypical carcinoid tumors account for 10-16% of all carcinoids, are more aggressive than typical carcinoids, and are more strongly associated with metastases to lymph nodes (57% versus 13%). Punctate, eccentric, or diffuse patterns of calcification have been described in 30% of cases. Hamartoma Hamartoma is the most common benign pulmonary neoplasm and is composed of connective tissue containing cartilage and varying amounts of fat, smooth muscle, bone, and lymphovascular structures. Approximately 6% of solitary pulmonary nodules identified on radiologic studies represent hamartomas. Hamartomas are characterized by slow growth, and malignant transformation is incredibly rare. Although a characteristic popcorn pattern of calcification has been described, it is only present in 10-15% of cases. Identification of both internal fat and calcium is virtually diagnostic of a hamartoma. Following the administration of intravenous contrast, most lesions demonstrate heterogeneous enhancement. Calcification has been described in 30% of cases and may manifest with diffuse, eccentric, or punctate patterns. Carcinoids may demonstrate intense enhancement following the administration of intravenous contrast. These findings are virtually diagnostic of hamartoma, and no further imaging or intervention is necessary. The lesion produces middle and right lower lobe atelectasis with intrinsic bronchiectasis distal to the endoluminal obstruction. Air-trapping often occurs due to proliferation of neuroendocrine cells in the airways. Chemotherapy &/or radiotherapy can be considered for symptom relief and disease control in patients with unresectable atypical carcinoid. Surgical pathology after pneumonectomy showed carcinoid tumor with rare mitoses, necrosis, and an infiltrative growth pattern suggesting atypical carcinoid. As is the case with gastrointestinal carcinoid tumors, the liver is the predominant site of metastatic disease. The patient underwent middle lobectomy for resection of the atypical carcinoid tumor and was found to have several ipsilateral subcarinal and middle lobe lymph nodes positive for metastatic disease. Atypical carcinoid is characterized by more than 2 mitoses per 10 high-power fields. More than 10 mitoses per 10 highpower fields confirms the diagnosis of high-grade neuroendocrine carcinoma. Typical and atypical carcinoid are lowand intermediate-grade malignancies respectively and are incidentally detected in 25% of cases. Bronchial obstruction from carcinoid may also cause distal atelectasis, consolidation, &/or airtrapping. Note the multiple soft tissue pleural nodules representing solid pleural metastases.

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