کانال علمی و پاسخ به شایعات وشبهات پزشکی

Infection associated with eosinophilia: عفونت های همراه با ائوزینوفیلی: A variety of infections may be associated with eosinophilia; these include helminths (worms), fungi, protozoa, bacteria, the retroviruses human immunodeficiency virus (HIV) and human T cell lymphotropic virus type 1 (HTLV-1), in addition to arthropod infestations, such as scabies (a mite infestation). Most acute bacterial infections and viral infections are not associated with eosinophilia. A clinical approach focusing on infectious causes of eosinophilia based on epidemiologic exposure and clinical manifestations is outlined below. In general, helminths are the most commonly identified infectious causes of eosinophilia . Categories of helminths include flukes (trematodes), tapeworms (cestodes), and roundworms (nematodes). The major helminth infections associated with eosinophilia are discussed below; additional information regarding helminths associated with eosinophilia is summarized in the table . Fungal infections classically associated with eosinophilia include allergic bronchopulmonary aspergillosis and coccidioidomycosis. Less commonly, peripheral eosinophilia has been reported in patients with histoplasmosis, paracoccidioidomycosis, cryptococcosis, and basidiobolomycosis. Protozoal infections associated with eosinophilia include cystoisosporiasis, sarcocystosis, and Dientamoeba fragilis. Bacterial infections associated with eosinophilia include bartonellosis, syphilis, and resolving scarlet fever. Mycobacterial infections associated with eosinophilia include tuberculosis and leprosy. In the setting of HIV infection, eosinophilia may occur as a result of concomitant opportunistic infection or in the context of an associated condition such as eosinophilic folliculitis or adrenal insufficiency . HTLV-1 infection has been associated with adult T-cell leukemia/lymphoma (ATL); ATL may be associated with eosinophilia in some circumstances [10]. In addition, HTLV-1 infection is a risk factor for disseminated. اپتودیت #strongyloidiasis. #eosinophilia #ائوزینوفیلی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

eosinophilia: ائوزینوفیلی: A variety of infections may be associated with eosinophilia; these include helminths (worms), fungi, protozoa, bacteria, the retroviruses human immunodeficiency virus (HIV) and human T cell lymphotropic virus type 1 (HTLV-1), in addition to arthropod infestations, such as scabies (a mite infestation). Most acute bacterial infections and viral infections are not associated with eosinophilia. A clinical approach focusing on infectious causes of eosinophilia based on epidemiologic exposure and clinical manifestations is outlined below. In general, helminths are the most commonly identified infectious causes of eosinophilia . Categories of helminths include flukes (trematodes), tapeworms (cestodes), and roundworms (nematodes). The major helminth infections associated with eosinophilia are discussed below; additional information regarding helminths associated with eosinophilia is summarized in the table . Fungal infections classically associated with eosinophilia include allergic bronchopulmonary aspergillosis and coccidioidomycosis. Less commonly, peripheral eosinophilia has been reported in patients with histoplasmosis, paracoccidioidomycosis, cryptococcosis, and basidiobolomycosis. Protozoal infections associated with eosinophilia include cystoisosporiasis, sarcocystosis, and Dientamoeba fragilis. Bacterial infections associated with eosinophilia include bartonellosis, syphilis, and resolving scarlet fever. Mycobacterial infections associated with eosinophilia include tuberculosis and leprosy. In the setting of HIV infection, eosinophilia may occur as a result of concomitant opportunistic infection or in the context of an associated condition such as eosinophilic folliculitis or adrenal insufficiency . HTLV-1 infection has been associated with adult T-cell leukemia/lymphoma (ATL); ATL may be associated with eosinophilia in some circumstances [10]. In addition, HTLV-1 infection is a risk factor for disseminated. اپتودیت #strongyloidiasis. #eosinophilia #ائوزینوفیلی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

Tetanus: کزاز: Because C. tetani will not grow in healthy tissues, a convergence of factors must be present in order for tetanus toxin to be elaborated in the human host. This combination of factors usually includes absence of antibodies (ie, from inadequate vaccination) plus two or more of the following: ●A penetrating injury resulting in the inoculation of C. tetani spores ●Coinfection with other bacteria ●Devitalized tissue ●A foreign body ●Localized ischemia The above factors explain why tetanus-prone injuries include splinters and other puncture wounds, gunshot wounds, compound fractures, burns, and unsterile intramuscular or subcutaneous injections (that often occur in injection drug users). These predisposing factors can also explain why tetanus can develop in unusual clinical settings such as in: ●Neonates (due to infection of the umbilical stump) ●Obstetric patients (after septic abortions) ●Postsurgical patients (with necrotic infections involving bowel flora) ●Adolescents and adults undergoing male circumcision in sub-Saharan Africa . ●Patients with dental infections ●Diabetic patients with infected extremity ulcers ●Patients who inject illicit and/or contaminated drugs Tetanus in patients without an identifiable cause:  — An identifiable antecedent cause for tetanus is obvious in most patients presenting with tetanus, but no cause can be identified in up to a quarter of patients with classic signs and symptoms of tetanus. Presumably, minor unnoticed abrasions or skin injuries are responsible for most or all of these "cryptogenic" cases. Tetanus has occurred rarely in patients who have received a timely and correct series of tetanus immunizations. اپتودیت #tetanus #کزاز تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

Discrepancies between acute phase reactant levels:  — Although elevations in multiple components of APR commonly occur together, not all happen uniformly in all patients. Discordance between concentrations of different APR is common; some may be elevated while others are not. Differences in the production of specific cytokines or their modulators in different diseases may account in large part for these variations . Additionally, as a patient’s condition worsens or improves, the ESR changes relatively slowly, while CRP concentrations can change rapidly. Discrepancies between ESR and CRP are found with some frequency. An elevated ESR observed together with a normal CRP is often a misleading result that may, for example, reflect the effects of blood constituents, such as monoclonal immunoglobulins, that are not related to inflammation but that can influence the ESR. It should not be routine practice to order serum protein electrophoresis (SPEP) and urine protein electrophoresis (UPEP) in such instances, unless the clinical presentation suggests that a plasma cell dyscrasia may be present. Systemic lupus erythematosus (SLE) represents an exception to the generalization that CRP concentrations correlate with the extent and severity of inflammation in patients with rheumatic disorders . The ESR may be elevated, sometimes markedly, in patients with active SLE, while the CRP response is muted. The muted CRP response in SLE appears to result from the ability of type I interferons, which are highly expressed in most lupus patients, to inhibit CRP induction in hepatocytes . While many patients with active SLE do not have significantly elevated CRP concentrations , CRP concentrations may be quite elevated in patients with active lupus serositis or with chronic synovitis . In a febrile lupus patient, marked CRP elevation (greater than 6 mg/dL) favors the diagnosis of bacterial infection . In a landmark study, infection was present in all patients with CRP levels over 6 mg/dL (60 mg/L) except for those with serositis, supporting the clinical utility of regarding marked CRP elevation as strongly suggestive of infection . Another more common example reflects the acuity of the acute phase response. CRP levels measure a single molecule, and one will note acute and rapid rise and fall with an insult. By contrast, because ESR is the reflection of numerous factors and the interaction of these elements (ie, long half-life of some plasma proteins), ESR levels do not rapidly rise at the beginning of an inflammatory insult; similarly, normalization is slower. This difference between ESR and CRP can help clinicians distinguish between acute processes and a more chronic process (for example, high CRP and normal ESR may suggest an acute paronychia; by contrast, elevated CRP and ESR may suggest osteomyelitis). In patients with active rheumatoid arthritis, the ESR and CRP generally tend to be parallel (ie, both are elevated or not elevated in a single patient). However, one study found that results for the two tests were discordant (ESR >28 mm/hr with CRP ≤0.8 mg/dL or ESR ≤28 mm/hr with CRP >0.8 mg/dL) in about one-quarter of patients with active rheumatoid arthritis in a large practice-based registry . Several studies have suggested that elevations of the acute phase protein procalcitonin are highly specific for infection ; thus, procalcitonin may prove useful in differentiating infections from other inflammatory stimuli in autoimmune disease patients . A 2012 systematic review and meta-analysis of nine observational studies that evaluated procalcitonin as a marker of infection in patients with autoimmune disease found that procalcitonin and CRP exhibited similar sensitivity for infection (75 versus 77 percent), but that procalcitonin had significantly higher specificity (90 versus 56 percent) .Thus, procalcitonin determination was inadequate to exclude infection. #CRP #ESR تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

خلاصه اي راجع به زردي نوزادان: زردي كه در هنگام تولد موجود بوده يا در خلال 24 ساعت اول زندگي تظاهر مي كند ممكن است در اثر اريتروبلاستوز فتاليس، خونريزي پنهان، سپتي سمي ، CMV ، سرخجه يا توكسوپلاسموز مادرزادي باشد. زردي روز دوم يا سوم تولد معمولا فيزيولوژيك است. ولي ممكن است در اثرانواع شديد تر هيپر بيليروبينمي نوزاد  باشد. سندرم كليگلر نجار ابتدا روز دوم يا سوم تولد ديده مي شود. زردي كه بعد از روز سوم و در خلال هفته اول تولد تظاهر كند احتمال سپتي سمي ویا عفونت ادراری را مطرح مي كند و ممكن است در اثر عفونتهاي ديگري مانند سيفليس ، توكسوپلاسموز، CMV ،آنتروویروس باشد . زردي ثانويه به اكيموز وسیع يا هماتوم ممكن است روز اول يا ديرتر تظاهر كند. شروع زردي بعد از هفته اول : زردي ناشي از شير مادر (breast milk jaundice)                          ، سپتي سمي، آترزي مادرزادي مجاري صفراوي ، هپاتيت ، سرخجه ، هپاتيت هرپسي ، گالاكتوزمي ، هيپوتيروئيديسم ، اسفروسيتوز ارثي ، كمبود آنزيمي گلبول قرمز يا آنمي هموليتيك در اثر داروها . زردي مداوم در خلال ماه اول تولد در اثر:    هپاتيت ، CMV ، سيفليس ،توكسوپلاسموز ، آترزي مادر زادي  مجاري صفراوي ،inspissated bile syndrome ،گالاكتوزمي است . در صورتيكه نوزاد هيپوتيروئيديسم يا استنوز پيلور داشته باشد زردي فيزيولوژيك ممكن است چند هفته طول بكشد. در موارد زير بايد براي پيداكردن علت زردي اقدام كرد : اگر زردي در 24 ساعت اول تولد پيداشده باشد . اگر بيليروبين سرم بيش از mg 5 درصد در 24 ساعت بالا برود . اگر بيليروبين سرم بيش از 12 ميلي گرم درصد در نوزاد فول ترم و بيش از 14-10 ميلي گرم درصد درنوزاد  نارس باشد . اگرزردي كه بعد از هفته دوم زندگي طول بكشد . اگر بيليروبين مستقيم در هر زمانی بالا باشد. سابقه فاميلي بيماري هموليتيك ، رنگ پريدگي ، هپاتومگالي ، اسپلنومگالي ، اگر بافتوتراپي زردي كاهش نيابد ، استفراغ ، لتارژي ، اگر نوزاد خوب شير نخورد ، اگر وزن قابل توجهي كم كند ،اگر آپنه ،برادي كاردي، هيپوترمي ، مدفوع رنگ پريده ، ادرار تيره كه بيليروبين آن مثبت باشد و یاعلائم كرن ايكتروس موجودباشد. زردي ناشی از تغذيه با شير مادر :breast milk jaundice بين روزهاي 4-7 بعداز تولد شروع مي شود و حداكثر 10-30 ميلي گرم درصد در خلال 2-3 هفته ممكن است برسد . زردي بتدريج كاهش يافته و سپس مدت 10-3 هفته  در سطح پائين تري ادامه ميابد . اگر 1-2روز شير مادررا  به نوزاد نداده و بجاي آن شير خشك بدهيم بيليروبين سرم سريعا كاهش مي یابد ولی اینکاررا بطور روتین بجز درمواردی که مقدار بیلیروبین اندازه ای باشد که ارزش اینکار را داشته باشدتوصیه نمیکنم زیرا در این نوع زردی با گذشت زمان بیلیروبین بتدریج بطرف نرمال سیر میکند وقطع شیر مادرهم اثر روانی ناخوشایندی روی مادر دارد وگاهی مادران تشویق میشوند تغذیه با شیر خشک را قطع نکرده وادامه دهند .بنابراین شیر مادر را ادامه میدهیم ولی نوزاد را از نظر مقداربیلیروبین فالو میکنیم ودرصورت لزوم در صورت بالا بودن بیلیروبین از فتوتراپي استفاده و شیر مادر را موقتا با شیرخشک برای دو روز جایگزین میکنیم که باعث کاهش بیلیروبین شده و با شروع شیر مادر دوباره به مقدار قبلی باز نمیگردد. اين سندرم بايستي از هيپر بيليروبينمي غير كنژوگه تسريع شده با شروع زودرس در هفته اول زندگي افتراق داده شود كه در آن شير مادر خواران بيليروبين بالاتري نسبت به نوزاداني كه شير خشك ميخورند دارند. اين نوزادان دريافت شيرشان از طرف مادر كم است. و دهيدراتاسيون وكمبود كالري پيدا مي كنند . اين نوزادان را نبايد با آب قند سير كرد و بايد مكررا شير داد تا از پيدايش زردي در آنها جلوگيري شود. به اين مسئله breast feeding jaundice مي گويند. #هیپربیلیروبینمی_نوزادی #زردی_ناشی_از_شیر_مادر تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

Ferritin is a marker of iron stores, but it may also be elevated as an acute phase reactant or due to massive cell and tissue death, especially in the liver and in the setting of hemophagocytosis. The absolute ferritin level cannot be interpreted in isolation and should not be the sole basis for treatment decisions. The pattern of ferritin increase (progressive, acute/marked increase, or chronic mild elevation) as well as the patient's underlying condition must be incorporated in the evaluation.

The differential diagnosis for TBG deficiency: includes central hypothyroidism and euthyroid sick syndrome. Laboratory testing for patients with central hypothyroidism shows low FT4, low Total T4 along with low or inappropriately normal TSH levels. Central hypothyroidism may be congenital or acquired. Some critically ill euthyroid patients with non-thyroidal illness may also present with low FT4, low T4 along with low TSH. However, most of these patients present with high reverse T3 levels due to reduced clearance of Reverse T3. These abnormalities usually resolve with resolution of non-thyroid illness.

Thyroxine-binding globulin (TBG): is one of three major transport proteins, which are primarily responsible for binding to and transporting thyroid hormones to the necessary tissues.  The other two serum transport proteins include transthyretin and human serum albumin.  While there are higher amounts of albumin in serum, TBG has a greater affinity to thyroxine (T4). Abnormalities in the functionality and amount of TBG can cause variations in the total amount of T4 in the serum, but not in the amount of bioactive free T4.  Since the amount of free T4 circulating in the serum remains the same, deficiency in thyroxine-binding globulin often does not lead to adverse metabolic effects seen in an individual with abnormal thyroid hormone levels. However, it can cause errors in the interpretation of thyroid hormone labs, which can ultimately lead to inappropriate treatment. Thyroxine-binding globulin (TBG) is a serine protease inhibitor produced in the liver. It belongs to the SERPINA7 family. The encoding gene for this protein is on the long arm of the X chromosome and as such, inherited forms of TBG tend to follow an X-linked pattern. Approximately 27 different mutations have been identified to play a role in the etiology of the inherited form of complete TBG deficiency thus far. These mutations seem to be caused by a nucleotide substation or by a frameshift.  Missense mutations have been the only type identified so far in an inherited form of partial TBG deficiency. Acquired forms of TBG deficiency are attributable to degradation and altered synthesis of the molecule. Patients with hyperthyroidism have been found to have an increase in the rate of turnover of TBG.  In terminal illness, interleukin-6 seems to play a role in altering the levels of TBG. Levels of TBG have been found to vary with fluctuations in sex hormones as well.  For example, estrogen has been known to cause an increase in TBG, while androgens have been found to decrease levels TBG. #thyroid #TBG #تیروئید تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

Neisseria gonorrhoeae treatment in adults: Neisseria gonorrhoeae is an important cause of sexually transmitted infections that can have severe reproductive health consequences. N. gonorrhoeae can rapidly develop antibiotic resistance. What is added by this report? Based on review of recent evidence, CDC recommends a single 500 mg intramuscular dose of ceftriaxone for uncomplicated gonorrhea. Treatment for coinfection with Chlamydia trachomatis with oral doxycycline (100 mg twice daily for و 7 days) should be administered when chlamydial infection has not been excluded. CDC #Neisseria gonorrhoeae تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles

 biliary atresia: آترزی صفراوی: All jaundiced infants and children with BA should be given supplements of fat-soluble vitamins . Once jaundice resolves and vitamins are replete, children can be transitioned to standard multivitamins. Nevertheless, routine monitoring of vitamin levels should continue. Vitamin levels should be monitored frequently (ie, several times in the first year), starting at the first month after HPE, in order to adjust supplements appropriately for deficiencies or toxicities. The frequency of laboratory monitoring depends in part on persistence or resolution of cholestasis. Deficiencies of fat-soluble vitamins are common in patients with BA. In a series of 29 patients with BA, serologic deficiencies of vitamins A and E and radiographic evidence of vitamin D deficiency were reported despite establishment of bile flow by HPE . Vitamin deficiencies occur despite recommended supplementation and are particularly common among patients with residual cholestasis after Kasai HPE (defined in this study as serum total bilirubin ≥2 mg/dL [34 micromol/L]) . In one study, 81 percent of infants were found to be vitamin D deficient before HPE and vitamin D deficiency persisted post-HPE despite aggressive supplementation . Infants with BA and prolonged jaundice may be deficient in vitamin K. Patients should receive supplementation with oral vitamin K and should be monitored for coagulopathy. Some infants may require parenteral vitamin K supplementation due to poor absorption of oral medications in the setting of severe cholestasis. #biliary_atresia #آترزی_صفراوی تهیه شده توسط : کانال مطالعات تخصصی طب کودکان با نظارت دکتر منصور شیخ الاسلام https://t.me/pediatricarticles