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I read this article with interest and, as a final year medical student, I am writing to add my thoughts to this growing area of discussion and describe how, in my experience, the situation has changed since 2014, when I started medical school and this article was published.
The authors of this article noted that talking openly about challenges people with mental health issues face could relieve negative effects of stigma and help change general attitudes. I believe we have made progress towards this over the past five years. During the first part of university, mental health awareness campaigns came from student unions, not the MedSoc or clinical school, and there was little specific emphasis on medical student welfare. Now, my clinical school consistently encourages its students to speak out if they are struggling and signposts professionals and services we can access if needed. Additionally, students and doctors are talking publicly about their struggles, such as the rise of blogs including the Depressed Medical Student, and research by the British Medical Association (BMA).
The article does not explore how the institutionalised pressure of medicine contributes to or exacerbates mental health problems. A BMA report showed that 90% survey respondents attributed their condition to the working or studying environment (“BMA - Supporting the mental health of doctors and medical students,” n.d.). In my pre-clinical years at medical school, we were pushed for academ...
I read this article with interest and, as a final year medical student, I am writing to add my thoughts to this growing area of discussion and describe how, in my experience, the situation has changed since 2014, when I started medical school and this article was published.
The authors of this article noted that talking openly about challenges people with mental health issues face could relieve negative effects of stigma and help change general attitudes. I believe we have made progress towards this over the past five years. During the first part of university, mental health awareness campaigns came from student unions, not the MedSoc or clinical school, and there was little specific emphasis on medical student welfare. Now, my clinical school consistently encourages its students to speak out if they are struggling and signposts professionals and services we can access if needed. Additionally, students and doctors are talking publicly about their struggles, such as the rise of blogs including the Depressed Medical Student, and research by the British Medical Association (BMA).
The article does not explore how the institutionalised pressure of medicine contributes to or exacerbates mental health problems. A BMA report showed that 90% survey respondents attributed their condition to the working or studying environment (“BMA - Supporting the mental health of doctors and medical students,” n.d.). In my pre-clinical years at medical school, we were pushed for academic excellence, sometimes at the expense of adequate sleep, a social life, or time to de-stress. I had friends openly state they would ‘sacrifice [their] mental health for a first class’ and spend all day with a textbook. However, during clinical school, pressure changed to be the pinnacle of professionalism as we are ‘held to a higher standard’. Suddenly family members would come to us with health questions and expect us to know the answers. The GMC was presented as a body to be feared, and stories circulated of doctors being struck off for admitting to mental illness – anecdotally, this seems to be one of the biggest barriers particularly for final year medical students to coming forward. However, this could be dispelled by blogs such as the Depressed Medical Student with people progressing through their careers despite struggles with mental health issues. Although I have yet to experience it, I imagine the pressure changes again for students after becoming FY1 doctors.
We are getting better at speaking up about mental illness, but there is a way to go before people can do so completely stigma-free. Furthermore, we have not successfully addressed the growing prevalence of mental health issues amongst medical students and doctors. To an extent, it is unavoidable, since medicine is inherently stressful, but maybe we could be doing more to support struggling doctors, particularly juniors who are most at risk.
The publication of a clinical case in the BMJ Case Report on March 8 [1], entitled "Anaphylaxis probably induced by transfer of amoxicillin via oral sex", has resulted in interest in social networks, local and national press, radio, and television, reporting with big headlines of such allergic reaction, but without contrasting the work assessing the scientific content and experimental support.
The article reports the case of a woman with a history of allergy to penicillin in childhood who, after having sexual intercourse (vaginal and oral) with her partner, who was being treated for otitis media with amoxicillin/clavulanic acid and ibuprofen, presents dyspnea, vomiting, and urticaria. The patient had not ingested any unusual food. She was diagnosed with anaphylaxis probably induced by amoxicillin/clavulanic acid transfer in the seminal fluid of the couple through oral sex. This diagnosis was based solely on a skin reaction suffered in her childhood after taking amoxicillin (no description of how that diagnosis was made) and a probability algorithm [2]. No allergological investigation was conducted at the time of the reaction.
Previous studies have shown that seminal fluid can serve as a route of transmission of ingested allergens, such as nut proteins [3], and drugs such as vinblastine [4], and penicillin [5]. The latter study was the only one in which intradermal tests with penicillin, with a positive result, and intra-epidermal tests with semen, w...
The publication of a clinical case in the BMJ Case Report on March 8 [1], entitled "Anaphylaxis probably induced by transfer of amoxicillin via oral sex", has resulted in interest in social networks, local and national press, radio, and television, reporting with big headlines of such allergic reaction, but without contrasting the work assessing the scientific content and experimental support.
The article reports the case of a woman with a history of allergy to penicillin in childhood who, after having sexual intercourse (vaginal and oral) with her partner, who was being treated for otitis media with amoxicillin/clavulanic acid and ibuprofen, presents dyspnea, vomiting, and urticaria. The patient had not ingested any unusual food. She was diagnosed with anaphylaxis probably induced by amoxicillin/clavulanic acid transfer in the seminal fluid of the couple through oral sex. This diagnosis was based solely on a skin reaction suffered in her childhood after taking amoxicillin (no description of how that diagnosis was made) and a probability algorithm [2]. No allergological investigation was conducted at the time of the reaction.
Previous studies have shown that seminal fluid can serve as a route of transmission of ingested allergens, such as nut proteins [3], and drugs such as vinblastine [4], and penicillin [5]. The latter study was the only one in which intradermal tests with penicillin, with a positive result, and intra-epidermal tests with semen, with a negative result, were carried out. In addition, seminal fluid-specific IgE levels were also determined, with a negative result [5].
In the present case, a relevant allergological study was not carried out at the time of the reaction in order to confirm the amoxicillin/clavulanic acid sensitization described by the patient, including in vivo and in vitro tests (skin tests, specific IgE levels or provocation tests to -lactam antibiotics). From the skin reaction after amoxicillin ingestion in childhood, it could be speculated that the patient is allergic to penicillins. However, this speculation has little experimental support. In the experience of most allergists, the cutaneous reactions produced in childhood, coinciding with the taking of penicillins, are usually infectious rashes. Neither skin tests nor determination of specific IgE to the semen have been carried out to rule out seminal plasma hypersensitivity (SPH) which, despite being a rare phenomenon, is more prevalent than the allergic reaction by drug transfer (amoxicillin), so it is necessary to rule out such a possibility [6]. It would also be necessary to rule out postcoital asthma or food allergy (it is not excluded that she has previously tolerated a food) through an in vivo and in vitro allergological study that includes the assessment of serum tryptase levels, other types of acute urticaria and even microorganisms, which in this case has not been investigated [7].
Although the prevalence of SPH is unknown, we believe that this pathology may be underdiagnosed. Currently, around 100 cases have been documented in the English literature, being more frequently between 20-30 years and occurring at first sexual intercourse in 40-50% of patients [8]. According to a survey conducted in 1997 to 1,073 US women, between 20,000-40,000 patients could suffer SPH (1/5,000) [9].
In Spain, the Allergy Unit of the General University Hospital of Elda published in 1993 the first case of immediate SPH, demonstrated by skin tests and determination of specific IgE positive to seminal plasma [10]. In December 2017, we published a second case of local SPH which, in turn, was the first case of local SPH with colposcopic and histopathological control after postcoital vulvovaginal exposure, as well as local manifestations (contact urticaria) after oral sex [11]. This work was the first case published in the literature of SPH demonstrated by genital biopsy and the first documented case of allergy to seminal fluid by oral sex. We also want to highlight the work carried out by Basagaña et al. describing the prostatic specific antigen (PSA) as one of the allergens that is sometimes responsible for SPH due to the cross-reactivity with Can f 5 allergen of dogs [12].
Therefore, it is desirable that scientific journals are keen to verify that published articles are supported by scientific evidence and solid experimental results, which make the "probable allergen" involved in the described allergic reaction very likely to be the "real allergen". This must always be taken into account, but even more so when the topic is very attractive for the general media to take the published information to look for eye-catching and sensational headlines. Of course, all the aforementioned information does not exclude that the allergic reaction was produced by amoxicillin transfer through the semen, but obviously it is necessary to have more experimental evidence to suggest it with certain guarantees of success. Articles should not be left in simple explanatory hypotheses without sufficient experimental evidence to support them.
REFERENCES
1. Gomez Caballero N, Almenara S, Tevar Terol A, Horga de la Parte JF. Anaphylaxis probably induced by transfer of amoxicillin via oral sex. BMJ Case Rep. 2019;12.
2. Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30:239-45.
3. Bansal AS, Chee R, Nagendran V, Warner A, Hayman G. Dangerous liaison: sexually transmitted allergic reaction to Brazil nuts. J Investig Allergol Clin Immunol. 2007;17:189-91.
4. Paladine WJ, Cunningham TJ, Donavan MA, Dumper CW. Letter: Possible sensitivity to vinblastine in prostatic or seminal fluid. N Engl J Med. 1975;292:52.
5. Green RL, Green MA. Postcoital urticaria in a penicillin-sensitive patient. Possible seminal transfer of penicillin. JAMA. 1985;254:531.
6. Shah A, Panjabi C. Human seminal plasma allergy: a review of a rare phenomenon. Clin Exp Allergy. 2004;34:827-38.
7. Nusair B, Gallagher E, Purohit P, Chye Gooi JH, Hamoda H. Seminal fluid hypersensitivity: A case report and review of the literature. Current Women's Health Reviews. 2018;14:81-6.
8. Resnick DJ, Chen L, Low J, Lee-Wong MF. Seminal plasma hypersensitivity and successful intravaginal graded challenge. Internet J Asthma Allergy Immunol. 2014;10.
9. Bernstein JA, Sugumaran R, Bernstein DI, Bernstein IL. Prevalence of human seminal plasma hypersensitivity among symptomatic women. Ann Allergy Asthma Immunol. 1997;78:54-8.
10. Jover Cerdá V, Parera M, Valera AC. Hipersensibilidad al fluido seminal humano: Presentación de un caso. Rev Esp Alergol Inmunol Clin Supl. 1993;8:223-7.
11. Jover Cerdá V, Rodríguez Pacheco R, Doménech Witek J, Durán García R, Garcia Teruel MJ, Santes García J, et al. Seminal plasma hypersensitivity: Clinical and histopathologic features in a multipara woman. J Allergy Clin Immunol Pract. 2017;5:1768-70.
12. Basagaña M, Bartolomé B, Pastor-Vargas C, Mattsson L, Lidholm J, Labrador-Horrillo M. Involvement of Can f 5 in a case of human seminal plasma allergy. Int Arch Allergy Immunol. 2012;159:143-6.
We read with interest the article by Bhandare and Ruchi (1). They diagnosed severe organic mercury (Hg) poisoning in a 69 year old man with known hypertension and diabetes who presented with a transient altered mental status. The diagnosis was based on a history of increased fish consumption and a blood Hg level of 35 ng/mL. Methylmercury (MeHg) is the form present in seafood, but there are multiple chemical forms of Hg and each has different health consequences. Everyone who consumes seafood is exposed to MeHg, but it is the dosage that is critical. The US EPA determined the MeHg reference dose (defined as “…a daily oral exposure …that is likely to be without an appreciable risk of deleterious effects during a lifetime”) to be 5.8 ng/mL in blood. That value was based on dividing the lowest observed adverse effect level of 58 ng/mL (a value reported from a large, controversial epidemiological study) by a safety factor of 10. Blood MeHg exposures of 35 ng/mL and higher are common, with no evidence of clinical symptoms. For example, residents of the Seychelles islands consume large amounts of marine fish, have documented blood MeHg exposures at or above 35 ng/mL, and are asymptomatic. A recent Seychelles study of 1,266 mothers reported that they ate fish with meals 8.5 ± 4.5 times per week while pregnant and had a mean blood Hg level of 18.2 ng/mL (2). The maximum blood Hg level in that study was 84.2 ng/mL and no mother reported clinical manifestations. The mean...
We read with interest the article by Bhandare and Ruchi (1). They diagnosed severe organic mercury (Hg) poisoning in a 69 year old man with known hypertension and diabetes who presented with a transient altered mental status. The diagnosis was based on a history of increased fish consumption and a blood Hg level of 35 ng/mL. Methylmercury (MeHg) is the form present in seafood, but there are multiple chemical forms of Hg and each has different health consequences. Everyone who consumes seafood is exposed to MeHg, but it is the dosage that is critical. The US EPA determined the MeHg reference dose (defined as “…a daily oral exposure …that is likely to be without an appreciable risk of deleterious effects during a lifetime”) to be 5.8 ng/mL in blood. That value was based on dividing the lowest observed adverse effect level of 58 ng/mL (a value reported from a large, controversial epidemiological study) by a safety factor of 10. Blood MeHg exposures of 35 ng/mL and higher are common, with no evidence of clinical symptoms. For example, residents of the Seychelles islands consume large amounts of marine fish, have documented blood MeHg exposures at or above 35 ng/mL, and are asymptomatic. A recent Seychelles study of 1,266 mothers reported that they ate fish with meals 8.5 ± 4.5 times per week while pregnant and had a mean blood Hg level of 18.2 ng/mL (2). The maximum blood Hg level in that study was 84.2 ng/mL and no mother reported clinical manifestations. The mean cord blood Hg level at birth in their children was 34.5 ng/mL (n = 935; maximum 181.3 ng/mL) and no clinical manifestations in the children were reported at age 7 years. In New York State, the Department of Health reported on 3,078 adults with blood Hg levels ≥ 15 ng/mL (3). Among them, 611 reported eating fish or seafood daily and that cohort had a mean blood Hg level of 30.8 ng/mL with maximum levels as high as 161 ng/mL (3). Confirmed MeHg poisoning from fish consumption has only been report following 2 major industrial pollution episodes in Japan over 50 years ago (4). The fish consumed in that poisoning had Hg levels as high as 117 ppm while commercial fish with only naturally acquired MeHg levels seldom exceed 1 ppm. Typical characteristics of MeHg poisoning include a delay of several weeks between exposure and symptoms, and clinical symptoms are generally considered irreversible. Thinking outside the box should be encouraged, but should be evidence based.
References
1. Bhandare D, Ruchi R. Unusual complication of an Alaskan cruise: thinking outside the box. BMJ Case Rep 2019; 12: e227727
2. Wahlberg K, Love TM, Pineda D, et al. Maternal polymorphisms in glutathione-related genes are associated with maternal mercury concentrations and early child neurodevelopment in a population with a fish-rich diet. Environment International 2018; 115: 142-149
3. Fletcher AM, Gelberg KH. An Analysis of Mercury Exposures among the Adult Population in New York State. J Community Health 2013; 38: 529-537
4. Yokoyama H. Mercury Pollution in Minamata. Springer Briefs in Environmental Science. Open Access: Singapore. 2018 pp 1-74
While I have not doubt there are incidents involving vascular migration of Implanon NXT, the presentation of this case study raises some interesting questions verging to concerns about the details:
1. As stated by the authors, the device measures 4 cm long and 2 mm diameters. The suggested radioopaque foreign body shown in Figure 1 and 2 appears to be disproportionately long. These images suggest the skeletal frame involving torso of the woman is no wider than 25-30 cm (bone-wise) which meant this is an extra-ordinarily small woman.
2. CT Chest reported ‘hyperdense image with 40 mm, compatible with Implanon in the anterior basal segment of the lower left lobe in intravascular topography'. Interestingly the authors stated that "Implanon was removed by video assisted thoracoscopic surgery without pulmonary resection. Surgical procedure and postoperative course had no complications. " As reader may be aware, video assisted thoracoscopic surgery (VATS) primarily involved the insertion of thoracoscopes into pleural cavities via small incision on the chest. It would have been helpful to know if the implanon device had been found in the pulmonary vasculature, lung tissue or actually in the pleural space itself. As reflected in the article's own reference (1) on an example of VATS retrieval, it is no simple matter.
The lack of such details in the article raises more questions than answers
While I have not doubt there are incidents involving vascular migration of Implanon NXT, the presentation of this case study raises some interesting questions verging to concerns about the details:
1. As stated by the authors, the device measures 4 cm long and 2 mm diameters. The suggested radioopaque foreign body shown in Figure 1 and 2 appears to be disproportionately long. These images suggest the skeletal frame involving torso of the woman is no wider than 25-30 cm (bone-wise) which meant this is an extra-ordinarily small woman.
2. CT Chest reported ‘hyperdense image with 40 mm, compatible with Implanon in the anterior basal segment of the lower left lobe in intravascular topography'. Interestingly the authors stated that "Implanon was removed by video assisted thoracoscopic surgery without pulmonary resection. Surgical procedure and postoperative course had no complications. " As reader may be aware, video assisted thoracoscopic surgery (VATS) primarily involved the insertion of thoracoscopes into pleural cavities via small incision on the chest. It would have been helpful to know if the implanon device had been found in the pulmonary vasculature, lung tissue or actually in the pleural space itself. As reflected in the article's own reference (1) on an example of VATS retrieval, it is no simple matter.
The lack of such details in the article raises more questions than answers
Reference
1. Thomas PA , Di Stefano D , Couteau C , et al . Contraceptive implant embolism into the pulmonary artery: thoracoscopic retrieval. Ann Thorac Surg 2017;103:e271–2.doi:10.1016/j.athoracsur.2016.08.094
Dear authors. The location of the needle was interscapular, but it does not mention the exact site since the interscapular would be the spine. Anyway, I think pneumothorax must have been arrived from puncturing a pleural bubble. More, was "bounce" maneuver stimulation performed with the needle? This maneuver entails numerous punctures of the bubble, facilitating the pneumothorax.
Dear Editor,
We read with interest the report in the present Journal of Edington M. et al [1] titled “Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS”.
Erectile disfunction drugs play a role increasing levels of cyclic guanosine monophosphate (cGMP) with subsequent effects on nitric-oxide release. This condition can lead to acute angle-closure glaucoma (AACG) in case of anatomical predisposition. AACG is an ophthalmic emergency, it can lead to irreversible blindness if not identified and treated immediately and precipitating factors include certain drugs as nitrates, bronchodilators, cough mixtures, cold and flu medication, antidepressants, antihistamines and anticonvulsants [2]. Furthermore, a precedent case of AACG following sildenafil citrated therapy is also described [3].
We would like underline that this situation could lead to more serious effects, that only the mild chemical ocular injury, in presence of ophthalmic structural diseases.
References:
1. Edington M, Connolly J, Lockington D. Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS. BMJ Case Rep. 2018 Dec 3;11(1). doi: 10.1136/bcr-2018-227468.
2. Murray D. Emergency management: angle-closure glaucoma. Community Eye Health. 2018;31(103):64.
3. Ramasamy B, Rowe F, Nayak H, Peckar C, Noonan C. Acute angle-closure glaucoma following sildenafil citrate-aided sexua...
Dear Editor,
We read with interest the report in the present Journal of Edington M. et al [1] titled “Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS”.
Erectile disfunction drugs play a role increasing levels of cyclic guanosine monophosphate (cGMP) with subsequent effects on nitric-oxide release. This condition can lead to acute angle-closure glaucoma (AACG) in case of anatomical predisposition. AACG is an ophthalmic emergency, it can lead to irreversible blindness if not identified and treated immediately and precipitating factors include certain drugs as nitrates, bronchodilators, cough mixtures, cold and flu medication, antidepressants, antihistamines and anticonvulsants [2]. Furthermore, a precedent case of AACG following sildenafil citrated therapy is also described [3].
We would like underline that this situation could lead to more serious effects, that only the mild chemical ocular injury, in presence of ophthalmic structural diseases.
References:
1. Edington M, Connolly J, Lockington D. Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS. BMJ Case Rep. 2018 Dec 3;11(1). doi: 10.1136/bcr-2018-227468.
2. Murray D. Emergency management: angle-closure glaucoma. Community Eye Health. 2018;31(103):64.
3. Ramasamy B, Rowe F, Nayak H, Peckar C, Noonan C. Acute angle-closure glaucoma following sildenafil citrate-aided sexual intercourse. Acta Ophthalmol Scand. 2007; 85: 229-230.
Influenza-induced rhabdomyolysis by Martin Brunnstrom et al 1 has called my attention because they refer to the patient's story "A man aged 29 years with a past medical history of cerebral palsy, seizures and chronic constipation".
The authors refer to "Other causes for rhabdomyolysis were investigated and excluded" and "A muscle biopsy ruling out an underlying metabolic myopathy or polymyositis to identify a risk factor for rhabdomyolysis was not obtained."
My comments are related to cerebral palsy and seizures.
Can these manifestations be warning signs of an underlying metabolic or mitochondrial disease?
Then the rhabdomyolysis could be a manifestation, for example of a mitochondrial disease exacerbated by an infection.
Cerebral palsy (CP) is defined by its nonprogressive features. Characterization of CP is traditionally based on the predominant quality of motor impairment (spastic, dyskinetic, ataxic-hypotonic or mixed, assessed on standard neurologic examination 2
A number of neurodegenerative, including metabolic and genetic disorders may present with similar symptoms and signs. 3
The presence of dyskinesia or spastic quadriplegic in clinical examination, in addition to abnormal findings in neuroimaging such as syrinx malformation, cerebellar hypoplasia, white matter paucity, and abnormal signal in basal ganglia may warrant further investigation for a disorder other than CP. As inborn errors...
Influenza-induced rhabdomyolysis by Martin Brunnstrom et al 1 has called my attention because they refer to the patient's story "A man aged 29 years with a past medical history of cerebral palsy, seizures and chronic constipation".
The authors refer to "Other causes for rhabdomyolysis were investigated and excluded" and "A muscle biopsy ruling out an underlying metabolic myopathy or polymyositis to identify a risk factor for rhabdomyolysis was not obtained."
My comments are related to cerebral palsy and seizures.
Can these manifestations be warning signs of an underlying metabolic or mitochondrial disease?
Then the rhabdomyolysis could be a manifestation, for example of a mitochondrial disease exacerbated by an infection.
Cerebral palsy (CP) is defined by its nonprogressive features. Characterization of CP is traditionally based on the predominant quality of motor impairment (spastic, dyskinetic, ataxic-hypotonic or mixed, assessed on standard neurologic examination 2
A number of neurodegenerative, including metabolic and genetic disorders may present with similar symptoms and signs. 3
The presence of dyskinesia or spastic quadriplegic in clinical examination, in addition to abnormal findings in neuroimaging such as syrinx malformation, cerebellar hypoplasia, white matter paucity, and abnormal signal in basal ganglia may warrant further investigation for a disorder other than CP. As inborn errors metabolism and mitocondrial diseases 4.
Some mitocondrial diseases underlying cerebral palsy 5
• Coenzyme Q10 deficiency: Spastic paresis; progressive ataxia and dystonia
• MELAS: Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like Episodes
• Pyruvate dehydrogenase deficiency: Spastic quadriplegia; dystonia
• Depletion Syndrome POLG1
Some disorders may be misdiagnosed as cerebral palsy 3:
• With apparent or real muscle weakness
• With significant dystonia/involuntary movements
• With predominant diplegia/tetraplegia
• With significant ataxia
References
1. Runnstrom M, Ebied AM, Khoury AP, Reddy R. Influenza-induced rhabdomyolysis. BMJ Case Rep. 2018;11:
2. Olney RS, Doernberg NS, Yeargin-Allsop M. Exclusion of Progressive Brain Disorders of Childhood for a Cerebral Palsy Monitoring System: A Public Health Perspective. J Registry Manag. 2014;41:182-9.
3. Appleton RE, Gupta R. Cerebral palsy: not always what it seems. Arch Dis Child 2001;85:356–360
4. Al-Jabri B, Goez H. Atypical Cerebral Palsy: Edmonton Experience. IJSR 2017;6: 1537-8
5. Leach EL, et al. Treatable inborn errors of metabolism presenting as cerebral palsy mimics: systematic literature review. Orphanet J Rare Dis. 2014;9:197
We wish to share our clinical experience and support the importance of long term monitoring of thyroid function in patients with central congenital hypothyroidism caused by maternal thyrotoxicosis. This is a case series of three infants with prolonged hypothyroxinaemia unrelated to the initial management of neonatal Graves’ disease (NGD). In contrast to the minimal antenatal care reported in the case report. mothers of all infants in our case series had antenatal diagnosis of Graves’ disease with appropriate management and close follow up for signs of fetal hyperthyroidism. All infants were diagnosed with NGD within two weeks of birth with two infants being commenced on antithyroid medication for 2-4 weeks as they were symptomatic with NGD.
With resolution of NGD, thyroid function tests were monitored with subsequent hypothyroxinaemia noted between 4-8 weeks of age. Having confirmed persistent hypothyroxinaemia, all infants were commenced on thyroxine (4-10mcg/kg/day) with regular follow up of their thyroid function tests.
The development of hypothyroxinaemia after initial treatment of NGD is uncommon however has been described previously (1). In most cases, NGD remits by 3-12 weeks once maternal antibodies are cleared (2, 3). Early transient hypothyroxinaemia in infants of poorly controlled maternal Graves’ is well reported due to high circulating antibodies particularly in the third trimester (1, 4). Postulated mechanisms include suppression of the pituita...
We wish to share our clinical experience and support the importance of long term monitoring of thyroid function in patients with central congenital hypothyroidism caused by maternal thyrotoxicosis. This is a case series of three infants with prolonged hypothyroxinaemia unrelated to the initial management of neonatal Graves’ disease (NGD). In contrast to the minimal antenatal care reported in the case report. mothers of all infants in our case series had antenatal diagnosis of Graves’ disease with appropriate management and close follow up for signs of fetal hyperthyroidism. All infants were diagnosed with NGD within two weeks of birth with two infants being commenced on antithyroid medication for 2-4 weeks as they were symptomatic with NGD.
With resolution of NGD, thyroid function tests were monitored with subsequent hypothyroxinaemia noted between 4-8 weeks of age. Having confirmed persistent hypothyroxinaemia, all infants were commenced on thyroxine (4-10mcg/kg/day) with regular follow up of their thyroid function tests.
The development of hypothyroxinaemia after initial treatment of NGD is uncommon however has been described previously (1). In most cases, NGD remits by 3-12 weeks once maternal antibodies are cleared (2, 3). Early transient hypothyroxinaemia in infants of poorly controlled maternal Graves’ is well reported due to high circulating antibodies particularly in the third trimester (1, 4). Postulated mechanisms include suppression of the pituitary-thyroid axis due to fetal hyperthyroxinaemia caused by transplacental transfer of thyroxine in untreated hyperthyroid mothers or of thyroid-stimulating immunoglobulin from the mother (4, 5). It is not surprising the longstanding effects of poorly controlled maternal Graves’ disease given the early effects on thyroid function, with TSH receptors becoming responsive to TSH and to TSH-receptor antibodies around 20 weeks (6) and the hypothalamic-pituitary-thyroid axis continues to mature from the second half of gestation until one to two months postnatal.
The role of thyrotropin receptor antibodies has also been reported in the ‘switching’ between hypothyroidism to hyperthyroidism or vice versa. McLachlan et al described that varying concentration and affinities of thyroid stimulating versus blocking antibodies and immunological effect associated with the primary disease itself could contribute to ‘switching’ (7). Recovery of TSH levels tend to be delayed and has been reported to take up to 3-19 months in childhood Graves and up to 3¼ years in treated NGD (4).
Hypothyroxinaemia post initial management of NGD is an uncommon entity in addition to the rare background occurrence of NGD, but requires early recognition so that appropriate treatment may be instigated. There are known risk factors that predict the development of NGD but from this case series, there were no obvious factors that suggested the subsequent development of hypothyroxinaemia. It raises the importance of frequent clinical monitoring of growth and development supported by ongoing screening of TFTs in NGD.
References
1. Papendieck P, Chiesa A, Prieto L, Gruneiro-Papendieck L. Thyroid disorders of neonates born to mothers with Graves' disease. J Pediatr Endocrinol Metab. 2009;22(6):547-53.
2. Levy-Shraga Y, Tamir-Hostovsky L, Boyko V, Lerner-Geva L, Pinhas-Hamiel O. Follow-up of newborns of mothers with Graves' disease. Thyroid : official journal of the American Thyroid Association. 2014;24(6):1032-9.
3. Kamishlian A, Matthews N, Gupta A, Filipov P, Maclaren N, Anhalt H, et al. Different outcomes of neonatal thyroid function after Graves' disease in pregnancy: patient reports and literature review. J Pediatr Endocrinol Metab. 2005;18(12):1357-63.
4. Matsuura N, Harada S, Ohyama Y, Shibayama K, Fukushi M, Ishikawa N, et al. The mechanisms of transient hypothyroxinemia in infants born to mothers with Graves' disease. Pediatric research. 1997;42(2):214-8.
5. Higuchi R, Kumagai T, Kobayashi M, Minami T, Koyama H, Ishii Y. Short-term hyperthyroidism followed by transient pituitary hypothyroidism in a very low birth weight infant born to a mother with uncontrolled Graves' disease. Pediatrics. 2001;107(4):E57.
6. Polak M, Le Gac I, Vuillard E, Guibourdenche J, Leger J, Toubert ME, et al. Fetal and neonatal thyroid function in relation to maternal Graves' disease. Best practice & research Clinical endocrinology & metabolism. 2004;18(2):289-302.
7. McLachlan SM, Rapoport B. Thyrotropin-blocking autoantibodies and thyroid-stimulating autoantibodies: potential mechanisms involved in the pendulum swinging from hypothyroidism to hyperthyroidism or vice versa. Thyroid : official journal of the American Thyroid Association. 2013;23(1):14-24.
Ewing sarcoma and primitive peripheral neuroectodermal tumor (PNET) are high-grade malignant tumours typically found in children and adolescents. These tumours belong to the family of small round cell tumours and are of neuro ectodermal origin Primary Ewing sarcoma (EWS) of the kidney is a rare tumor in adults. It was first described in 1975 by Seemayer and colleagues, and has since been sporadically documented in the literature Ewing sarcoma and primitive peripheral neuroectodermal tumor (PNET) were originally described as two distinct pathologic entities, although both share common stem-cell precursor and unique chromosomal abnormality. Because of their similar histologic and cytogenetic characteristics, these tumors are now considered part of a spectrum of neoplastic diseases now known as Ewing’s sarcoma family tumors (ESFT), which also includes other malignancies The ESFT are most common in bone. Extraskeletal ESFT are less common and can affect the skin, soft tissue, or viscera So Renal primary sarcomas are a rare group of renal tumours. Ewing sarcoma/PNET of the kidney is distinctly rare, with more than 100 cases reported globally. Among these, leiomyo sarcoma is the most common (40–60%) followed by lipo sarcoma (10–15%) Sources of renal EWS include neural cells that invaginate into the kidney during its development some authors theorize that embryonic neural crest cells migrate into the kidney and undergo tumorigenesis It is primarily a genetic disease with case...
Ewing sarcoma and primitive peripheral neuroectodermal tumor (PNET) are high-grade malignant tumours typically found in children and adolescents. These tumours belong to the family of small round cell tumours and are of neuro ectodermal origin Primary Ewing sarcoma (EWS) of the kidney is a rare tumor in adults. It was first described in 1975 by Seemayer and colleagues, and has since been sporadically documented in the literature Ewing sarcoma and primitive peripheral neuroectodermal tumor (PNET) were originally described as two distinct pathologic entities, although both share common stem-cell precursor and unique chromosomal abnormality. Because of their similar histologic and cytogenetic characteristics, these tumors are now considered part of a spectrum of neoplastic diseases now known as Ewing’s sarcoma family tumors (ESFT), which also includes other malignancies The ESFT are most common in bone. Extraskeletal ESFT are less common and can affect the skin, soft tissue, or viscera So Renal primary sarcomas are a rare group of renal tumours. Ewing sarcoma/PNET of the kidney is distinctly rare, with more than 100 cases reported globally. Among these, leiomyo sarcoma is the most common (40–60%) followed by lipo sarcoma (10–15%) Sources of renal EWS include neural cells that invaginate into the kidney during its development some authors theorize that embryonic neural crest cells migrate into the kidney and undergo tumorigenesis It is primarily a genetic disease with cases affected sporadically, mainly a translocation type of mutation causing a fusion between the EWS gene on chromosome 22 and FLI1 on chromosome
Mean age at diagnosis of 30.4 years with the majority being male. Presentation of such tumors reported in the literature is non-specific and frequently involves localised pain which usually involves flank, subcostal or abdominal area with or without hematuria Differential diagnosis include Renal cell carcinoma and Wilm’s tumor ; neuroblastoma; malignant lymphoma ;metastatic renal involvement from sarcoma elsewhere in the body
No specific signs of PNET have been described in ultra sonography, computed tomography (CT), or magnetic resonance imaging (MRI). The imaging characteristics of most renal sarcomas are indistinguishable from those of RCC . These tumors appears as ill-defined, large heterogeneous masses with necrotic and hemorrhagic areas. Using ultrasonography, the tumour appears isoechogenic or hyperechogenic to the renal parenchyma. The CT findings include areas of internal haemorrhage or necrosis, peripheral hyper vascularity, and diffuse calcification. On MRI, the tumour appeared iso intense or hypo intense on T1-weighted images but heterogeneous intermediate to high T2 signal intensity . Venous extension into the renal vein, inferior vena cava, and right heart has been described .
Biopsy of the kidney mass show that Ewing sarcoma/primitive neuroectodermal tumor The pathologic findings shows usually multiple areas of necrosis and haemorrhage. In some cases, the tumour may exhibits calcifications and can be surrounded by a fibrous capsule. Microscopic features associated with ESFT/PNET are considered however non-specific as they can be seen in many other tumors, hence, the use of immunochemistry with CD99 over expression and cytogenetic analysis for definitive diagnosis Diagnosis is to be confirmed by fluorescence in situ hybridization (FISH) technique, which showed translocations involving the EWS locus (EWSR1 gene rearrangement).
The terms Pancoast tumors, superior sulcus tumors, and superior pulmonary sulcus tumors are applied to neoplasms located at the apical pleuro pulmonary groove. In 1924, Henry K. Pancoast, described a patient afflicted with a lung carcinoma occupying the apical thoracic cavity that was associated with a constellation of symptoms that included shoulder pain radiating down the arm, atrophy of the hand muscles, and Horner’s syndrome.[ 1] Since then, it has become widely accepted that the term Pancoast syndrome can be applied to any clinical condition in which a neoplasm in the apex of a lung is accompanied by shoulder or arm pain. Anatomically, the definition includes any tumor invading through the parietal pleura at the level of the first rib and above. The pulmonary sulcus refers to the costo vertebral gutter extending from the first rib to the diaphragm. The superior pulmonary sulcus is therefore analogous to the superior most portion of this recess. The first rib is at the base of the thoracic inlet. The thoracic inlet contains the subclavian vein anteriorly, the subclavian artery, phrenic nerve and trunks of the brachial plexus medially, and the nerve roots of the brachial plexus and the stellate ganglion posteriorly. The bony thorax in the superior sulcus includes the upper ribs and the associated vertebral bodies. It is invasion of this complex anatomical area that accounts for the classic symptoms of the Pancoast tumor. Superior sulcus carcinomas have the same biologic...
The terms Pancoast tumors, superior sulcus tumors, and superior pulmonary sulcus tumors are applied to neoplasms located at the apical pleuro pulmonary groove. In 1924, Henry K. Pancoast, described a patient afflicted with a lung carcinoma occupying the apical thoracic cavity that was associated with a constellation of symptoms that included shoulder pain radiating down the arm, atrophy of the hand muscles, and Horner’s syndrome.[ 1] Since then, it has become widely accepted that the term Pancoast syndrome can be applied to any clinical condition in which a neoplasm in the apex of a lung is accompanied by shoulder or arm pain. Anatomically, the definition includes any tumor invading through the parietal pleura at the level of the first rib and above. The pulmonary sulcus refers to the costo vertebral gutter extending from the first rib to the diaphragm. The superior pulmonary sulcus is therefore analogous to the superior most portion of this recess. The first rib is at the base of the thoracic inlet. The thoracic inlet contains the subclavian vein anteriorly, the subclavian artery, phrenic nerve and trunks of the brachial plexus medially, and the nerve roots of the brachial plexus and the stellate ganglion posteriorly. The bony thorax in the superior sulcus includes the upper ribs and the associated vertebral bodies. It is invasion of this complex anatomical area that accounts for the classic symptoms of the Pancoast tumor. Superior sulcus carcinomas have the same biologic behavior as lung carcinomas located in the lung parenchyma. Consequently, their diagnosis, staging, and treatment follow the same principles as for any other lung cancer. The unique characteristics of Pancoast tumors are related to the anatomy of the region where these tumors occur (thoracic inlet) and not to their biologic behavior.
Epidemiology
Pancoast tumors are a relatively rare subset of non-small cell lung cancers (NSCLC), accounting for fewer than 5% of all lung cancers. At least 50% of cases are histologically seen as adenocarcinomas, while the rest are squamous cell and large-cell carcinomas. Small cell carcinoma occurs rare. Patients often present with complaints of pain distributed to the upper anterior chest wall. These tumors may manifest with signs and symptoms related to the compression or infiltration of the middle and lower trunks of the brachial plexus such as shoulder and arm pain (in the distribution of the C8, T1, and T2 dermatome). The peripheral location of these tumors minimizes standard lung cancer symptoms such as cough, hemoptysis, and dyspnea and is the main reason why patients with Pancoast tumors present at a later stage of diagnosis . Diagnosis is established through biopsy of the mass. Given their location, these lesions are amenable to CT or ultrasound-guided fine-needle aspiration. Because of the peripheral location of the tumor, fiberoptic bronchoscopy is only able to establish the diagnosis in less than 30% of cases (unless there is nodal involvement). A tissue diagnosis via video-assisted thoracoscopy (VATS) may be indicated when other investigations are negative and to eliminate the possibility of pleural metastatic disease. Axillary minithoractomy is an alternative to VATS to obtain a tissue diagnosis of the mass in small apical tumors.
As with other lung carcinomas located in the lung parenchyma, it is imperative to stage the mediastinum with Pancoast tumors. Metastases to the mediastinal nodes is a major negative prognostic factor — 5-year survival rates in the presence of N2 disease are below 10%.4 According to the 2013 ACCP guidelines, before surgery for Pancoast tumors, an endobronchial ultrasound with transbronchial needle aspiration or a cervical mediastinoscopy is warranted to exclude N2/N3 disease, even in the absence of involved nodes in CT or PET scans. Pancoast tumors are by definition T3 or T4 tumors. Most of the lesions are classified as T3 tumors because they invade only the chest wall and/or the sympathetic chain. The rest invade brachial plexus, vertebral bodies, and vascular structures, and are classified as T4 tumors. According to the new staging system for lung cancer developed by the International Association for the Study of Lung Cancer (IASLC), their final stage, in the absence of distant metastases, depends on the N status of the tumor:
IIB if T3NO,
IIIA if T3N1-2, or T4NO-1,
IIIB if T3N3 or T4N2-3.
Therefore, even the earliest of these lesions are staged at least IIB. Invasion of the ipsilateral supraclavicular nodes in the setting of lung cancer is classified as N3 disease. In superior sulcus carcinomas the importance of supraclavicular node involvement is quite different because it is considered to represent a locoregional lymph node extension.
References
1] Pancoast H.K. Superior pulmonary sulcus tumor. JAMA. 1932;99:1391.
I read this article with interest and, as a final year medical student, I am writing to add my thoughts to this growing area of discussion and describe how, in my experience, the situation has changed since 2014, when I started medical school and this article was published.
Show MoreThe authors of this article noted that talking openly about challenges people with mental health issues face could relieve negative effects of stigma and help change general attitudes. I believe we have made progress towards this over the past five years. During the first part of university, mental health awareness campaigns came from student unions, not the MedSoc or clinical school, and there was little specific emphasis on medical student welfare. Now, my clinical school consistently encourages its students to speak out if they are struggling and signposts professionals and services we can access if needed. Additionally, students and doctors are talking publicly about their struggles, such as the rise of blogs including the Depressed Medical Student, and research by the British Medical Association (BMA).
The article does not explore how the institutionalised pressure of medicine contributes to or exacerbates mental health problems. A BMA report showed that 90% survey respondents attributed their condition to the working or studying environment (“BMA - Supporting the mental health of doctors and medical students,” n.d.). In my pre-clinical years at medical school, we were pushed for academ...
The publication of a clinical case in the BMJ Case Report on March 8 [1], entitled "Anaphylaxis probably induced by transfer of amoxicillin via oral sex", has resulted in interest in social networks, local and national press, radio, and television, reporting with big headlines of such allergic reaction, but without contrasting the work assessing the scientific content and experimental support.
The article reports the case of a woman with a history of allergy to penicillin in childhood who, after having sexual intercourse (vaginal and oral) with her partner, who was being treated for otitis media with amoxicillin/clavulanic acid and ibuprofen, presents dyspnea, vomiting, and urticaria. The patient had not ingested any unusual food. She was diagnosed with anaphylaxis probably induced by amoxicillin/clavulanic acid transfer in the seminal fluid of the couple through oral sex. This diagnosis was based solely on a skin reaction suffered in her childhood after taking amoxicillin (no description of how that diagnosis was made) and a probability algorithm [2]. No allergological investigation was conducted at the time of the reaction.
Previous studies have shown that seminal fluid can serve as a route of transmission of ingested allergens, such as nut proteins [3], and drugs such as vinblastine [4], and penicillin [5]. The latter study was the only one in which intradermal tests with penicillin, with a positive result, and intra-epidermal tests with semen, w...
Show MoreWe read with interest the article by Bhandare and Ruchi (1). They diagnosed severe organic mercury (Hg) poisoning in a 69 year old man with known hypertension and diabetes who presented with a transient altered mental status. The diagnosis was based on a history of increased fish consumption and a blood Hg level of 35 ng/mL. Methylmercury (MeHg) is the form present in seafood, but there are multiple chemical forms of Hg and each has different health consequences. Everyone who consumes seafood is exposed to MeHg, but it is the dosage that is critical. The US EPA determined the MeHg reference dose (defined as “…a daily oral exposure …that is likely to be without an appreciable risk of deleterious effects during a lifetime”) to be 5.8 ng/mL in blood. That value was based on dividing the lowest observed adverse effect level of 58 ng/mL (a value reported from a large, controversial epidemiological study) by a safety factor of 10. Blood MeHg exposures of 35 ng/mL and higher are common, with no evidence of clinical symptoms. For example, residents of the Seychelles islands consume large amounts of marine fish, have documented blood MeHg exposures at or above 35 ng/mL, and are asymptomatic. A recent Seychelles study of 1,266 mothers reported that they ate fish with meals 8.5 ± 4.5 times per week while pregnant and had a mean blood Hg level of 18.2 ng/mL (2). The maximum blood Hg level in that study was 84.2 ng/mL and no mother reported clinical manifestations. The mean...
Show MoreDear Editors
While I have not doubt there are incidents involving vascular migration of Implanon NXT, the presentation of this case study raises some interesting questions verging to concerns about the details:
1. As stated by the authors, the device measures 4 cm long and 2 mm diameters. The suggested radioopaque foreign body shown in Figure 1 and 2 appears to be disproportionately long. These images suggest the skeletal frame involving torso of the woman is no wider than 25-30 cm (bone-wise) which meant this is an extra-ordinarily small woman.
2. CT Chest reported ‘hyperdense image with 40 mm, compatible with Implanon in the anterior basal segment of the lower left lobe in intravascular topography'. Interestingly the authors stated that "Implanon was removed by video assisted thoracoscopic surgery without pulmonary resection. Surgical procedure and postoperative course had no complications. " As reader may be aware, video assisted thoracoscopic surgery (VATS) primarily involved the insertion of thoracoscopes into pleural cavities via small incision on the chest. It would have been helpful to know if the implanon device had been found in the pulmonary vasculature, lung tissue or actually in the pleural space itself. As reflected in the article's own reference (1) on an example of VATS retrieval, it is no simple matter.
The lack of such details in the article raises more questions than answers
Reference
Show More1. Th...
Dear authors. The location of the needle was interscapular, but it does not mention the exact site since the interscapular would be the spine. Anyway, I think pneumothorax must have been arrived from puncturing a pleural bubble. More, was "bounce" maneuver stimulation performed with the needle? This maneuver entails numerous punctures of the bubble, facilitating the pneumothorax.
Dear Editor,
We read with interest the report in the present Journal of Edington M. et al [1] titled “Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS”.
Erectile disfunction drugs play a role increasing levels of cyclic guanosine monophosphate (cGMP) with subsequent effects on nitric-oxide release. This condition can lead to acute angle-closure glaucoma (AACG) in case of anatomical predisposition. AACG is an ophthalmic emergency, it can lead to irreversible blindness if not identified and treated immediately and precipitating factors include certain drugs as nitrates, bronchodilators, cough mixtures, cold and flu medication, antidepressants, antihistamines and anticonvulsants [2]. Furthermore, a precedent case of AACG following sildenafil citrated therapy is also described [3].
We would like underline that this situation could lead to more serious effects, that only the mild chemical ocular injury, in presence of ophthalmic structural diseases.
References:
Show More1. Edington M, Connolly J, Lockington D. Prescribing lessons from an ocular chemical injury: Vitaros inadvertently dispensed instead of VitA-POS. BMJ Case Rep. 2018 Dec 3;11(1). doi: 10.1136/bcr-2018-227468.
2. Murray D. Emergency management: angle-closure glaucoma. Community Eye Health. 2018;31(103):64.
3. Ramasamy B, Rowe F, Nayak H, Peckar C, Noonan C. Acute angle-closure glaucoma following sildenafil citrate-aided sexua...
Influenza-induced rhabdomyolysis by Martin Brunnstrom et al 1 has called my attention because they refer to the patient's story "A man aged 29 years with a past medical history of cerebral palsy, seizures and chronic constipation".
Show MoreThe authors refer to "Other causes for rhabdomyolysis were investigated and excluded" and "A muscle biopsy ruling out an underlying metabolic myopathy or polymyositis to identify a risk factor for rhabdomyolysis was not obtained."
My comments are related to cerebral palsy and seizures.
Can these manifestations be warning signs of an underlying metabolic or mitochondrial disease?
Then the rhabdomyolysis could be a manifestation, for example of a mitochondrial disease exacerbated by an infection.
Cerebral palsy (CP) is defined by its nonprogressive features. Characterization of CP is traditionally based on the predominant quality of motor impairment (spastic, dyskinetic, ataxic-hypotonic or mixed, assessed on standard neurologic examination 2
A number of neurodegenerative, including metabolic and genetic disorders may present with similar symptoms and signs. 3
The presence of dyskinesia or spastic quadriplegic in clinical examination, in addition to abnormal findings in neuroimaging such as syrinx malformation, cerebellar hypoplasia, white matter paucity, and abnormal signal in basal ganglia may warrant further investigation for a disorder other than CP. As inborn errors...
We wish to share our clinical experience and support the importance of long term monitoring of thyroid function in patients with central congenital hypothyroidism caused by maternal thyrotoxicosis. This is a case series of three infants with prolonged hypothyroxinaemia unrelated to the initial management of neonatal Graves’ disease (NGD). In contrast to the minimal antenatal care reported in the case report. mothers of all infants in our case series had antenatal diagnosis of Graves’ disease with appropriate management and close follow up for signs of fetal hyperthyroidism. All infants were diagnosed with NGD within two weeks of birth with two infants being commenced on antithyroid medication for 2-4 weeks as they were symptomatic with NGD.
With resolution of NGD, thyroid function tests were monitored with subsequent hypothyroxinaemia noted between 4-8 weeks of age. Having confirmed persistent hypothyroxinaemia, all infants were commenced on thyroxine (4-10mcg/kg/day) with regular follow up of their thyroid function tests.
The development of hypothyroxinaemia after initial treatment of NGD is uncommon however has been described previously (1). In most cases, NGD remits by 3-12 weeks once maternal antibodies are cleared (2, 3). Early transient hypothyroxinaemia in infants of poorly controlled maternal Graves’ is well reported due to high circulating antibodies particularly in the third trimester (1, 4). Postulated mechanisms include suppression of the pituita...
Show MoreEwing sarcoma and primitive peripheral neuroectodermal tumor (PNET) are high-grade malignant tumours typically found in children and adolescents. These tumours belong to the family of small round cell tumours and are of neuro ectodermal origin Primary Ewing sarcoma (EWS) of the kidney is a rare tumor in adults. It was first described in 1975 by Seemayer and colleagues, and has since been sporadically documented in the literature Ewing sarcoma and primitive peripheral neuroectodermal tumor (PNET) were originally described as two distinct pathologic entities, although both share common stem-cell precursor and unique chromosomal abnormality. Because of their similar histologic and cytogenetic characteristics, these tumors are now considered part of a spectrum of neoplastic diseases now known as Ewing’s sarcoma family tumors (ESFT), which also includes other malignancies The ESFT are most common in bone. Extraskeletal ESFT are less common and can affect the skin, soft tissue, or viscera So Renal primary sarcomas are a rare group of renal tumours. Ewing sarcoma/PNET of the kidney is distinctly rare, with more than 100 cases reported globally. Among these, leiomyo sarcoma is the most common (40–60%) followed by lipo sarcoma (10–15%) Sources of renal EWS include neural cells that invaginate into the kidney during its development some authors theorize that embryonic neural crest cells migrate into the kidney and undergo tumorigenesis It is primarily a genetic disease with case...
Show MoreThe terms Pancoast tumors, superior sulcus tumors, and superior pulmonary sulcus tumors are applied to neoplasms located at the apical pleuro pulmonary groove. In 1924, Henry K. Pancoast, described a patient afflicted with a lung carcinoma occupying the apical thoracic cavity that was associated with a constellation of symptoms that included shoulder pain radiating down the arm, atrophy of the hand muscles, and Horner’s syndrome.[ 1] Since then, it has become widely accepted that the term Pancoast syndrome can be applied to any clinical condition in which a neoplasm in the apex of a lung is accompanied by shoulder or arm pain. Anatomically, the definition includes any tumor invading through the parietal pleura at the level of the first rib and above. The pulmonary sulcus refers to the costo vertebral gutter extending from the first rib to the diaphragm. The superior pulmonary sulcus is therefore analogous to the superior most portion of this recess. The first rib is at the base of the thoracic inlet. The thoracic inlet contains the subclavian vein anteriorly, the subclavian artery, phrenic nerve and trunks of the brachial plexus medially, and the nerve roots of the brachial plexus and the stellate ganglion posteriorly. The bony thorax in the superior sulcus includes the upper ribs and the associated vertebral bodies. It is invasion of this complex anatomical area that accounts for the classic symptoms of the Pancoast tumor. Superior sulcus carcinomas have the same biologic...
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