A 16-year-old boy presented with extensive lymphadenopathy, fever, weight loss, and decreased appetite for one month. There was no significant past medical or surgical history. On physical examination, multiple, firm to hard, lobulated and irregular lesions, ranging in size from 1.5 to 6.0 cm, were palpable at the cervical, supraclavicular, umbilical, and both right and left lumbar regions. No hepatomegaly or splenomegaly was noted. Complete blood count, renal and liver function tests, alpha-fetoprotein (AFP) and beta-human chorionic gonadotropin (β hCG) levels were normal. Chest X-ray showed evidence of pneumonitis, and no mediastinal widening was observed. An abdominal ultrasound revealed extensive abdominal adenopathy suggestive of lymphoma. Fine needle aspiration cytology (FNAC) of the cervical lesion was suggestive of a high-grade large-cell lymphoma. Cervical lymph node and bone marrow biopsies were performed one day before the patient’s death. The cervical lesion was excised and sent for histopathological examination.
On histology, the lymph node showed complete effacement of its architecture by diffuse proliferation of large-sized pleomorphic neoplastic cells ().
These cells had large, multilobated nuclei, coarse vesicular nuclear chromatin, and prominent nucleoli with abundant amount of eosinophilic cytoplasm. Large multinucleated cells were also noted (A and B). Numerous lymphocytes and few neutrophils interspersed these tumor cells. Frequent atypical mitotic figures were also noted.
An extensive panel of immunohistochemical markers was done (), which showed a strong positive reaction for CD68, CD4, vimentin, and weak positivity for CD45 and S-100 protein (). EBV-LMP1 was negative. The Ki-67 index was 60%.
The tumor cells were negative for PanCK and EMA, which ruled out carcinoma. Negativity for PLAP, SALL4 and OCT4 ruled out germ cell tumor, negativity for CD30 and ALK protein ruled out anaplastic large cell lymphoma, negativity for TdT, CD3, CD5, CD7, CD20, CD56, and PAX5 ruled out lymphoblastic lymphomas, negativity for MPO and CD117 ruled out myeloid sarcomas, negativity for CD1a, Langerin, CD21 and CD35 ruled out dendritic origin tumors, negativity for HMB-45, MelanA and Sox10 ruled out melanoma, and negativity for desmin ruled out rhabdomyosarcoma.
Bone marrow aspiration and biopsy were obtained, both of which showed cellularity of over 80% with a diffuse infiltration by the large pleomorphic cells as described earlier in the lymph node biopsy. All three hematopoietic cell lineages were suppressed. The immunohistochemistry profile of the bone marrow biopsy was similar to the findings in the lymph node biopsy. The histiocytic origin of the tumor was confirmed by the positive reaction of the tumor cells for CD68 (clone KP1) ().
The patient died from respiratory failure probably due to infection. The diagnosis was made posthumously on the basis of lymph node biopsy and immunohistochemistry taken just before his death. The autopsy of the patient was not performed as the deceased’s next of kin refused to authorize the procedure due to religious reasons.


A 66-year-old man was admitted into the general surgery department with intermittent abdominal pain. Abdominal CT revealed a soft tissue mass measuring 101 × 69 × 87 mm and extending along the left lower abdominal peritoneal space (). Plain CT revealed an irregular homogeneous low-density mass and surrounding lymph node enlargement (). In the arterial phase, numerous blood vessels were observed surrounding the mass. In the venous and delayed phases, the enhancement was seen to extend from the periphery to the center ().
The patient had a >10-year history of a mass on the left abdomen with intermittent pain. The patient could not provide the exact size of the tumor. His abdominal pain was relieved after rest and was not accompanied by diarrhea, constipation, nausea, vomiting, hematemesis, or other abnormalities. However, his abdominal pain had worsened 20 days previously. His stool and urine were normal, and there had been no significant change in his weight recently. The patient had previously undergone an operation involving the vertebrae and ribs as a result of trauma.
Hematological parameters, biochemical parameters and tumor marker levels (CA125, CA19-9, CA72-4, alpha-fetoprotein, and carcinoembryonic antigen) were normal. Surgical exploration revealed a firm mass in the left abdominal region. The mass originated from the mesojejunum and was enclosed by omental adhesions. Therefore complete tumor resection and partial omentectomy were performed to ensure safe surgical margins. Gross examination of the tumor revealed an incomplete fibrous envelope. Histopathological analysis of the mass revealed spindle-shaped cells with hypocellular and hypercellular regions rich in collagen (). Cellular atypia, pleomorphism, and necrosis were observed. Immunohistochemical analysis revealed that the mass was positive for CD34, STATA6, CD99, and vimentin () and negative for DOG1, her-2, p53, S-100, and CD117. The mass was also negative for pan-cytokeratin and smooth muscle actin, and the Ki-67 index was 40% (), indicating that the tumor cells were actively growing in some areas. The surgical margins were clear. The patient was discharged 1 week after surgery without complications and remained disease-free at the end of his 4-month clinical follow-up period.


A 61-year-old man with psoriasis since the age of 32 years and a past medical history of family hypercholesterolemia was hospitalized in May 2018 with fever (40°C), pharyngitis, and general malaise. On physical examination, enlargement of the spleen, liver, and lymph nodes was observed. Biochemical analysis revealed a white cell count of 12,000/mm3, elevations of hepatic transaminases (aspartate aminotransferase [AST] 120 IU/L, alanine aminotransferase [ALT] 111 IU/L) and the presence of atypical lymphocytosis. Human immunodeficiency virus (HIV), hepatitis B virus (HBV), hepatitis C virus (HCV), Epstein-Barr virus (EBV), CMV, and anti-neutrophil cytoplasmic autoantibodies (ANCA) serology screenings were performed in order to exclude any underlying cause, with normal results, except for IgM anti-CMV > 30 UA/mL. A diagnosis of acute CMV infection was made.
The patient was observed over time, and four weeks later his clinical manifestations disappeared and his blood tests returned to normal. One year later, the patient was referred to our department. On dermatological examination, we observed many erythematous-squamous plaques on his bilateral lower limbs, lumbar area, back, and trunk. These clinical features suggested the diagnosis of moderate-to-severe psoriasis, with a Psoriasis Area and Severity Index (PASI) score of 16, body surface area (BSA) score of 12 and a Dermatology Life Quality Index (DLQI) score of 18 ( and ). The patient had previously been treated with topical steroid therapy, ultraviolet (UV)B narrow-band phototherapy for about a year before discontinuing due to lack of efficacy, and treatment with 20 mg of methotrexate per week for about three years before stopping because of poor response. Taking this into account, the patient was eligible for therapy with biological agents, and considering the positive anamnesis for CMV infection, a careful screening was carried out; the patient did not have any clinical symptoms or sign of viral infection syndrome at the time of screening, and results were all within the normal range, except for IgM anti-CMV > 28 UA/mL and positive IgG anti-CMV. Considering these results, the patient had a consultation with the infectious disease specialist to determine if it was a new infection or a reactivation. Subsequently, IgG anti-CMV avidity and CMV-polymerase chain reaction (PCR) were ordered, with negative results. Having established that it was a previous infection, the infectious disease specialist determined that the patient could undertake therapy with a biological drug while monitoring IgG anti-CMV avidity and CMV-PCR every three months. In June 2019, after informed consent was obtained, we started treatment with secukinumab, an anti-interleukin-17A monoclonal antibody approved for the treatment of moderate-to-severe plaque psoriasis, at a dose of 300 mg by subcutaneous injection with initial dosing at weeks 0, 1, 2, 3 and 4, followed by monthly maintenance dosing. A good clinical response was obtained after 16 weeks of secukinumab (PASI 2, BSA 0, DLQI 0) ( and ) and was maintained during a 6-month follow-up. No infectious disease or reactivation of CMV infection or other adverse events were observed during the follow-up period. IgG anti-CMV avidity and CMV-PCR were negative after three, six, nine, and twelve months from starting therapy.


The patient was a 44-year-old female with G6P2 (spontaneous delivery once, cesarean section once, and induced abortion four times). Five months previously, the patient underwent uterine curettage in another hospital due to “50+ days of amenorrhea as well as RPOC in the uterine cavity.” The postoperative pathological examination findings indicated a less number of placental villi and a large amount of decidual tissue. Two months previously, uterine curettage was performed again in another hospital due to “RPOC in the uterine cavity and HCG 1301 mIU/ml.” Postoperative Pathological results showed that there were no placental villi and trophoblast cells, but a small amount of degenerative smooth muscle tissue and broken endometrial tissue. The transvaginal ultrasound result at our hospital indicated distinguishable inferior endometrium, but the middle and upper endometria were unclear. There was a heterogeneous hyperechogenic mass with a clear boundary at the size of approximately 6.2 cm × 6.6 cm × 6.4 cm in the middle to the upper uterine segment. Several irregular liquid dark areas were detected in the mass, with a maximum diameter of 4.3 cm []. Point-like or line-like blood flow signals were detected around and inside the mass, Resistance Index (RI) = 0.41 []. Thoracic and abdominal enhanced computed tomography (CT) results were as follows: cystic and solid space-occupying lesions in the uterine cavity, with a clear flocculent heterogeneous enhancement in the right uterine wall and fundus uteri, reaching deep into the musculature. There were low-density focuses in the anterior and posterior uterine walls, and one in the anterior wall reached the serosa layer, suggesting trophoblastic tumors []. In addition, a small nodule shadow of unknown nature appeared in the inner side of the middle lobe of the right lung []. The patient's serum HCG level was 547.9 mIU/ml.
Following three courses of diagnostic chemotherapy with (Etoposide+Methotrexate+Actinomycin D+cyclophosphamide) (MEA-CO), the serum HCG level decreased to 172.6 mIU/ml, while the uterine mass did not shrink. Therefore, hysteroscopy and hysterectomy were performed. The postoperative pathological examination results were as follows: the gross specimen revealed a dissected, spheric dark brown mass of 6.5 cm × 5.5 cm × 4.5 cm in the posterior wall of the uterus. A layer of opalescent translucent membranous tissue roughly 0.1 cm thick attached on the surface of the section, resembling the fetal membranes. Part of the area of the shape of a half-moon, approximately 5 cm × 2.5 cm, had peeled off []. The section of the mass was map-like, showing extensive hemorrhage and necrosis, and of fragile texture. The mass invaded nearly the entire muscular wall. Pathological microscopy showed a large number of highly degenerative or fibrotic placental villi in the tissue of hemorrhage and necrosis in the muscular wall of the uterine floor and body []. No trophoblastic tumors were detected.


We obtained the written informed consent to publication from the parent of the patient for this case report because the patient had slight mental retardation.
A 24-year-old man, with a height of 190 cm and weight of 52 kg, was admitted to our hospital with right neck of femur fracture to undergo closed reduction and internal fixation. He was diagnosed with WHS after birth. Although he had slight mental retardation, he was able to ambulate and perform simple commands. No specific problems were noted on the transthoracic echocardiography, although ventricular premature beats were present on the preoperative electrocardiogram. His blood tests and chest X-ray did not show any abnormal findings.
On the physical examination, the patient had facial features identical to patients with typical WHS. The Greek warrior’s helmet appearance, characterized by a prominent glabella, hypertelorism, micrognathia, low-set malformed ears, and a down-turned mouth, was present (). Although mouth opening was more than 3 fingers and neck extension had no limitation, his mandible was small and relatively pushed backward (). His tooth alignment and dental hygiene was under poor condition, and Mallampati score was class II. He had undergone an inguinal herniorrhaphy under general anesthesia two years prior without any complications. The information about the previous general anesthesia was limited because it was dependent on the memory from patient’s mother, but any complication has not occurred during anesthetic management including endotracheal intubation. However, as a long anterior-posterior diameter of chest was noticed on computed tomography (), difficult intubation and airway management were anticipated.
After entering the operating room, the hemodynamic status of the patient was stable with blood pressure of 115/91 mmHg, heart rate of 80 beats/min, and oxygen saturation of 99%. Total intravenous anesthesia was administered with 2% propofol and remifentanil to avoid malignant hyperthermia that has been previously reported during anesthesia of patients with WHS []. We injected 50 mg, about 1.0 mg/kg, of rocuronium intravenously while the neuromuscular transmission was monitored, considering that the usual duration of surgery is about one and a half hours or maximally two hours, the patient had no muscular hypotonia, and his mask ventilation was not challenging. As difficult intubation was anticipated, a video-assisted laryngoscope, C-MAC with D-blade (Karl Storz, Germany) was used, and endotracheal intubation with 7.5 sized reinforced endotracheal tube was delivered smoothly. The operation terminated without any problems under total intravenous anesthesia. Total duration of general anesthesia was one and a half hours and operation time was one hour. The endotracheal tube was extubated as soon as spontaneous breathing was recovered with intravenous administration of 200 mg of sugammadex, and the ratio of train of four was confirmed to be more than 90%. For reducing postoperative pain, 50 µg of intravenous fentanyl was administered with patient-controlled intravenous analgesia at the end of the operation. The patient was discharged on the thirteenth postoperative day without any complications.


In late 2017, a 61-year-old female patient visited the clinic for regular follow-up. The patient’s consciousness was clear, but with dullness and impaired cognitive function.
In 2013, the patient was brought to the emergency department after losing control of her bike because of sudden-onset right-sided limb weakness. The physical examination revealed a glasgow coma scale (GCS) of nine (E3M5V1). Brain computed tomography showed left putaminal intracranial hemorrhage, intraventricular hemorrhage, and hydrocephalus. Following surgical interventions, the patient (GCS of 14 [E4M6V4]) was discharged and transferred to another hospital for rehabilitation. In the following four years, the patient continuously received intensive rehabilitation therapy. Although her deep tendon reflex increased during follow-up, the patient’s right-sided hemiparesis remained and continuously affected her right dominant side.
The patient had a history of hypertension and hyperglyceridemia.
The patient’s physical examination revealed no remarkable findings.
The glucagon stimulation test showed a significantly reduced GH (< 3 μg/L).


A 31-year-old male with a positive clinical history of Cluster of Differentiation 4 (CD4) immunodeficiency, episodic joint pain, migraine and night sweats was admitted to our hospital for a suspected muscular disease. He reported to be an athlete participating in events like marathons. During marathon training, the patient experienced fatigue, cramps, and muscle fasciculations in the lower limbs (>gastrocnemius). Blood screening, including creatine phosphokinase (CPK), resulted to be within the normal range. At the presentation, neurological examination revealed mild hypotrophy of periscapular muscles (symmetric), right quadriceps femoris and left tibialis anterior. Pes cavus was absent. The strength was conserved. The muscle tone was normal. Brisk and irradiating tendon biceps and brachio-radial reflexes bilaterally, hyporeflexia of triceps, pronator teres and Achilles reflexes bilaterally, and brisk in patellar reflex bilaterally were also noted. No signs of upper motor neuron were present. No pain or alteration of sensitivity were reported, nor any history of facial nerve injury. Electromyography (EMG) revealed the presence of chronic neurogenic denervation with increased duration and amplitude 6/7 millivolt (mV) (collateral re-innervation) of motor unit potentials (MUP), some polyphasic potentials, reduced motor-unit recruitment during maximal voluntary contraction (reduced number of motor units) as reduced by axonal loss in the four limbs (proximal e distal muscles) and craniofacial district. In addition, EMG showed fasciculation potentials and acute denervation (slightly fibrillations and positive sharp waves) in the gastrocnemius muscles, just slightly fibrillations and positive sharp waves in extensor digitorum communis. No apparent gradient of greater gravity proximal/distal was revealed. Upper limbs appeared less severely affected than lower limbs. Brain and spinal cord Magnetic Resonance Imaging (MRI) resulted normal. The clinical symptoms resolved in about 2 months after the interruption of the competitive physical activity (see Table).
The multiplex ligation-dependent probe amplification (MLPA) was performed using the SALSA P021-A2, P060-A1 kits and P460-A1 from MRC-Holland. Analysis of MLPA data was performed using Software Coffalyser NET by MRC-Holland (Amsterdam, The Netherlands; ). P021-A2 contained a probe mixture for SMN1 exons 7 and 8, SMN2 exons 7 and 8 and several control fragments located on different chromosomes. P460-A1 probemix included probes for the rare allele of two polymorphisms of this SMN1 haplotype: g.27134T>G and g.27706-27707delAT. These probes do not give a signal on the great majority of DNA samples tested. A signal is usually present in samples that contain three or four SMN1 copies. Whether two probes give a signal on a sample that has only two copies of SMN1, there is an increased risk, in accordance to the ethnic background, that the person tested is a silent SMA carrier who carries two SMN1 copies on one allele and none on the other. The MLPA analysis performed on the patient with the P460-A1 kit (confirmed with MLPA P021-A2) showed two copies of exon 7-8 of the SMN1 gene with the absence of both copies of SMN2 gene. The analysis of marker loci close to the gene (g.27134T>G and g.27706-27707delAT) suggested the possibility of being a “silent carrier” (2+0). The two copies of SMN1 in cis were inherited from the mother. Therefore, we considered the patient and his mother as healthy carriers of SMA with only one functional copy (SMN1) in one of the two alleles. However, the patient produced only one full-length active transcripts, without the contribution, even if minimum (~20%), of the SMN2 full-length active transcripts (high copy number of SMN2 modulated, as it is known, clinical severity among SMA patients with homozygous deletion of SMN1). Moreover, the healthy mother showed two SMN2 copies [SMN1 (2+0) and SMN2 (two copies)] acting as a carrier. The healthy father reported two SMN1-SMN2 copies. We supposed that a de novo rearrangement was occurring in paternal meiosis, as described in other patients (2%)[]. In addition, research of deletion/duplication in 17p11.2 region performed with MLPA (P033-B4), resulted negative, ruling out the possibility of Charcot Marie Tooth disease type 1 (CMT1). The Clinical Exome Solution by SOPHiA GENETICS was performed following the protocol in the Thermo Fisher Scientific NGS machine, covering 4493 genes related to the most common inherited diseases, including amyotrophic lateral sclerosis and neuropathies. NGS detected heterozygous missense mutations of LRSAM1 (c.1298C>T, p.Ser433Leu) and RTN2 (c.764G>T, p.Cys255Phe) genes inherited from the mother. Finally, the Ion AmpliSeq Human Gene Expression Kit panel was used to analyze gene-level expression. Barcoded cDNA library was generated with SuperScript VILO™ cDNA Synthesis kit from 10 ng of total RNA (from peripheral blood). Then cDNA was amplified using Ion AmpliSeq™ technology of following targeted possible candidate genes implicates in phenotype: AIFM1, ATP7A, BSCL2, CCNA2, CMT1, FBXO38, GARS, HARS, HMN6, HSPB1, HSPB3, HSPB8, LAS1L, LRSAM1, PLS, RBM7, RTN2, SMN1, SMN2, TRPV4, UBE1, VRK1, WARS. Amplified cDNA of patient (SMN1=2+0; SMN2=0 copies) was compared to a healthy control (SMN1=1+1; SMN2=2 copies). Four independent experiments for patient and control were pooled equally (diluted to 100pM) and amplified using emulsion PCR on Ion Torrent CHEF instrument and enriched following manufactures instructions. Templated libraries were then sequenced on ION S5plus (Thermo Fischer) sequencing system, using 520 chip, obtaining >800K sequences for each.
Differential expression analysis was performed based on the difference in gene counts between the patient and control using Transcriptome Analysis Console (TAC). A gene was considered differentially expressed if it had a p-value less than 0.05 and an absolute log2 fold change greater than or equal to two. Only SMN2, as expected (patient=0 copies and control=2 copies), was found differentially expressed. Finally, the SMN1 fold change between the patient (SMN1=2+0) and control (SMN1=1+1), showed fold change -1.75 (p-value=0.0197) suggesting a decrease in expression probably compatible with the genotype (two copies in cis). This data should be verified in other individuals with SMN1 (1+0 or 2+0) and SMN2=0 copies; however this genotype is rare in our population (more than two hundred subjects analyzed).


A healthy old female aged 65 was referred to our department suffering from an atrophic non-union of the right humerus with a clear hardware loosening and massive bone loss complaining a stiff painful shoulder and referring three previous surgeries to her arm. All limited movements of her arm were located at the non-union site. Her medical history started on September 2012 when, because of diaphyseal humeral fracture, she was treated with an intramedullary reamed retrograde nail. On April 2013, because of a non-union at the fracture site, with a clear loosening of the proximal locking screws (fig 1a), she was treated with nail removal, debridement of the non-union and new fixation with a 9 holed 3.5 LCP plate using an extended antero-lateral approach to the humerus. On December 2013, because of proximal plate and screws loosing without any clear sign of bone healing (fig 1b), she underwent a third surgery with new debridement, autologous bone graft from iliac crest and repositioning of a new 9 holes plate adding 3 metallic cerclages to the construct to increase stability. On February 2015, the patient was referred to our institution because a catastrophic situation: more than 9 cm of diaphyseal bone loss (grade 3 according to Non-Union Scoring System – NUSS) () with a complete loose hardware palpable under the skin, and a reabsorbed humeral head, supposing a necrotic process (fig 2a, 2b). Clinically, the patient was extremely depressed and feed up for the unsuccessful previous treatments. She was complaining a stiff painful shoulder with a residual movement through the non-union site despite no evident peripheral neurological deficit.
At our institution, she was assessed to exclude any infection and all the blood tests, ultrasound guided biopsy with white cells count, and cultures from the non-union site were all negative despite a positive labeled leukocyte scintigraphy performed few weeks before our department admission. The shoulder status was assessed using a CT scan, showing visible reabsorption areas of the necrotic bone (fig 3b) and an evident previous nail hole in the metaphyseal region below the humeral head (fig 3a).
On April 2015, all hardware was removed in association together with debridement and a wide (11 cm) diaphyseal bone resection replaced by an handmade antibiotic loaded spacer (Gentamicin + Clindamycin) (fig 4). All the intraoperative specimens, including the removed hardware and cultures, resulted negative for any infection.
Two months later, the patient underwent the final surgical procedure with antibiotic spacer removal, debridement and a further 1+1 cm bone resection, and implanting a custom made cemented megaprosthesis (Megasytem-C, Waldemar Link, Hamburg, Germany). At 20 months postoperatively, the patient was extremely satisfied with a pain-free recovery to an almost normal lifestyle including car driving despite an incomplete shoulder range of motion recovery (<110° in shoulder elevation/abduction). At the radiological assessment, there were no radiological sign either of implant loosening or glenoid reabsorption or proximal migration of the humeral head (fig 5).


A 49-year-old woman came to the Outpatient Service of our hospital complaining of a cough, chest discomfort and fatigue on January 20, 2020.
The patient's symptoms started 5 d ago with a cough, expectoration and chest congestion.
She mentioned a travel history to Wuhan one week ago, the center of this CoVID-19 outbreak.
On admission, symptoms of cough, expectoration of white sputum, chest congestion and fatigue were observed, but her body temperature was normal 37.0°C (98.6°F). Coarse breath sounds in both lungs with wet rales distributed at the base of both lungs were heard on auscultation.
Laboratory studies showed a normal leukocyte count (white blood cell count, 5.58 × 109/L) and normal lymphocyte count (lymphocyte count, 1.47 × 109/L). The leukocyte differential count indicated 64.9% neutrophils, 26.3% lymphocytes, and 5.9% monocytes. There were elevated blood levels of C-reactive protein (12.50 mg/L) and erythrocyte sedimentation rate (37 mm/h). Albumin (32.1 g/L) and serum calcium (3.26 mmoL/L) were lower. Immunoglobulin M (IgM) antibody of Mycoplasma pneumoniae was positive (Table ).
Unenhanced chest computed tomography (CT) showed ground-glass opacities in bilateral lower lobes and a patchy and striate shadow in the right upper lobe. According to these findings and due to her travel history to Wuhan, we speculated that she had Mycoplasma infection and suspected SARS-CoV-2 infection; therefore, we sent a throat swab for analysis and the results were expected to take several days. Considering her CT images and the rapid development of CoVID-19, we treated the patient with anti-inflammatory and empirical antiviral drugs in the first three days. CT images showed progressive manifestations.
Three days later, real-time fluorescence polymerase chain reaction (RT-PCR) of sputum was positive for SARS-CoV-2 nucleic acid and her diagnosis of CoVID-19 was finally made based on laboratory results, chest CT images, clinical manifestations and epidemiologic characteristics. We were glad that we performed early intervention with antiviral therapy based on the previous CT manifestations.
CT showed multiple patchy ground-glass opacities and consolidated opacities in bilateral lower lobes (Figure ) and a patchy and striate shadow of slightly high density in the upper right lung (Figure ). This asymmetrical lesion in the upper right lobe was quite rare in the cases reported so far.


A 30-year-old man was admitted to our hospital with a mass in his occipital region for 1 mo.
One month prior to admission, the patient had found a mass, the size of which was approximately 1 cm × 1 cm, in the left occipital region and he did not consider it to be serious. One month later, the patient found that the mass was enlarged, so he presented to the hospital.
The patient was in good health prior to the present illness.
The patient had no previous or family history of similar illnesses.
Physical examination showed a mass in the left occipital area of the patient, approximately 2 cm × 2 cm in size, that was rigid and had no associated tenderness.
The laboratory examinations (including routine blood and urine tests, coagulation function tests, liver and kidney function tests, and tumor markers) were normal.
Computed tomography (CT) examination showed a left occipital nodule with a subcutaneous diameter of approximately 2 cm, a uniform density, and a CT value of approximately 25 Hu. The nodule boundary was clear, the edge was smooth (Figure ), and there was no destruction of the adjacent skull bone (Figure ). Magnetic resonance imaging (MRI) showed an oval subcutaneous nodule in the left occipita, and the lesion showed iso-signal intensity on T1-weighted imaging (T1WI). The nodule grew close to the superficial fascia of the left occipita to the subcutaneous fat layer, and the edge was clear and smooth (Figure ). T2-weighted imaging (T2WI) showed inhomogeneous high signal intensity in the lesion, and the central signal was higher than that of the periphery (Figure ). A contrast-enhanced scan of the lesion showed obvious inhomogeneous enhancement, and the peripheral enhancement was higher than that of the center, showing an inverted target sign (Figure ). The sagittal contrast-enhanced scan of the lesion showed obvious thickening and enhancement of the adjacent fascia, showing a fascial tail sign (Figure ).
Postoperative pathology showed that a large number of proliferated spindle cells were arranged erratically, and myxoid matrix, local angiogenesis, and a small amount of erythrocyte extravasation could be seen (Figure ). Immunohistochemistry showed positive expression of SMA in spindle cells in the lesion (Figure ).


A 12-year-old girl presented to the Pediatric Dermatology Clinic for a 6-year history of asymptomatic linear plaques on her knee. She was not known for any diseases and didn’t take any medication. The patient had no systemic symptoms such as fever, weight loss, arthralgias, oral ulcers, photosensitivity, or cardiopulmonary symptoms. Atrophic, squamous, and erythemato-violaceous plaques following Blaschko’s lines were noted on her left knee (). Antinuclear antibodies (ANA), extractable nuclear antigen (ENA) antibodies (full panel including anti-SSA, anti-SSB, anti-Sm, anti-RNP, anti-Scl-70, anti-Jo-1 and anti-CENP-B), and anti-double stranded DNA (anti-dsDNA) antibodies were negative. Laboratory tests such as complete blood count, creatinine, urinalysis, liver tests, and C-reactive protein were normal.
Skin biopsy revealed vacuolar interface dermatitis with superficial and deep lymphohistiocytic perivascular and periadnexal infiltrates, lymphocytic vasculitis and increased dermal mucin deposition (). Direct immunofluorescence (DIF) was not done. Little response was noted under betamethasone dipropionate 0.05% cream. Hydroxychloroquine (5 mg/kg/day) combined with tacrolimus 0.1% ointment led to a significant improvement within 6 months.


A healthy 15-year-old boy presented a 3-year history of slightly pruriginous linear lesions on his thigh. There were no systemic symptoms, and a review of systems was negative. Blaschkoid squamous and erythemato-violaceous papules with follicular plugging were observed on his left anterior and medial thigh (). ANA, ENA full panel and anti-dsDNA were negative, and the remaining laboratory investigations were normal. Skin biopsy showed findings similar to the first patient (). DIF was not done. Complete resolution was noted within 5 months under hydroxychloroquine (5 mg/kg/day) with clobetasol propionate 0.05% cream (for 5 weeks), followed by tacrolimus 0.1% ointment.


A 91-year-old woman presented unconscious after experiencing a heat stroke while working outside. Her health was normal before the onset of heat stroke; she was transferred to our hospital 5 h after the onset. She was undergoing hyperlipidemia treatment with 5 mg/day of atorvastatin calcium hydrate. Physical examination of the patient revealed a deep coma; the blood pressure, pulse, and respiratory rate were 73/48 mmHg, 135 bpm, and 24 breaths/min, respectively. Her axillary body temperature was 40.7°C, while the core temperature was 39.8°C in the bladder; she weighed 45 kg. Laboratory investigations revealed elevated lactate levels and disseminated intravascular coagulation (DIC) due to heat stroke; however, infection-related tests, such as white blood cell count, C-reactive protein, and procalcitonin were normal (Table ). A computed tomography (CT) scan of the head, thorax, abdomen, and pelvis with contrast indicated cerebral atrophy and dilatation of the gallbladder and digestive tract; it did not identify emphysematous changes. Consequently, the patient was diagnosed with a heat stroke.
We immediately performed tracheal intubation and cooled the body by spraying cold water and cold fluid infusion. The patient’s core temperature lowered to <38°C, while the systolic pressure recovered to >100 mmHg for 90 min. Although the immediate cooling and stabilization of circulation was successful, the lactate level improved only marginally. We treated her with massive fluid infusion and anti-DIC therapy (17,100 U/day of thrombomodulin alfa and 1,500 U/day of antithrombin III) due to the prolonged shock and DIC. The patient was treated for 24 h with 6,200 mL of fluid infusion; the total urinary output was 1,800 mL with acute diarrhea (Fig. ).
After 22 h of arrival at our hospital, the patient’s blood pressure decreased to 72/50 mmHg, while her fever increased to 40.6°C (Fig. ). Although the physical examination of right upper quadrant abdominal pain and signs of peritoneal irritation was unclear, an abdominal X-ray examination indicated emphysematous cholecystitis (Fig. ). We diagnosed the patient with septic shock resulting from emphysematous cholecystitis and performed emergency cholecystectomy. During the surgery, the gallbladder revealed ischemic changes, including edema, dark red coloration, and emphysematous changes on its wall. Inflammation of the gallbladder affected the neighboring liver and duodenum (Fig. ).
Although stable following the cholecystectomy, the patient experienced disuse syndrome. She suffered from DIC and acute kidney and hepatic injury presented as complications of heat stroke. She recovered as a result of anti-DIC therapy and massive fluid infusion until day 5 of hospitalization. As the bile culture was positive for Clostridium perfringens, we continued to administer 1.5 g/day of meropenem starting from the day after cholecystectomy to day 7 and 9 g/day of sulbactam/ampicillin until day 14. On day 12, the patient indicated signs of Clostridium difficile colitis and was administered 0.5 g/day of oral vancomycin, which was continued until day 25. On day 13, mechanical ventilation management was terminated; on day 32, the patient was transferred for rehabilitation.


A 42-year-old male with known HBV (diagnosed in Romania in 2011) presented to North Middlesex Hospital with deranged LFTs in September 2013. He did not drink alcohol or have any risk factors for non-alcohol related fatty liver disease (NAFLD). Subsequent investigations revealed a diagnosis of HBV-HDV co-infection, and histopathology was consistent with advanced fibrosis (Ishak stage 5) with severe portal inflammation. Viral loads of both viruses were detectable with HBV DNA of 39 iU/ml (e-antigen negative/e-antibody positive at presentation) and a rising HDV RNA of 6.5 × 106 iU/ml going up to 8.8 × 106 iU/ml.
Treatment with Pegylated interferon-alpha 3 was initiated in April 2014, and an initial encouraging response was documented with HDV RNA down to 220 iU/ml after 14 weeks of treatment. After 6 months, HBV DNA was undetectable and after 8 months, HDV RNA was also undetectable. The patient completed 12 months of treatment before unfortunately being lost to follow up and therefore SVR was not assessed.
Two years later, aged 45, he presented to Luton & Dunstable University hospital with a transaminitis (ALT 61). Although the liver looked radiologically unremarkable, a subsequent Fibroscan indicated F2 fibrosis (7.2 kPa). In addition, viral loads of both viruses had become detectable again (HDV RNA 77 iU/ml, HBV DNA 30 iU/ml). The suspicion that both viruses working in tandem were causing progressive liver damage prompted treatment with a second course of Pegylated interferon-alpha 2a (Pegasys).
Following this second course (which the patient stopped at 6 months due to non-compliance) he was essentially cured of his Hepatitis delta infection (HDV RNA undetectable, HDV IgM negative) with an SVR 12 months after completion of treatment (see graph 1). Furthermore, although Hepatitis B surface antigen remains positive and therefore functional cure has not been achieved, he became a very low level chronic HBV carrier (HBV DNA undetectable) as a result of the treatment. Finally, persistent biochemical normalization has been achieved.


Mrs S. was a 25-year-old married Caucasian woman when she presented herself the first time to us at the clinic’s trauma consultation centre for a preliminary examination, without previous psychotherapeutic treatment. The pregnant woman (13th week of gestation) already had a two-year-old daughter. At the time of hospitalization, Mrs S. was pregnant in the 21st week of pregnancy.
She had suffered from symptoms like intrusions, nightmares and irritability in social situations for a long time following CSA by a close relative between the age of five and ten as well as a substantial emotional neglect by her mother. Furthermore, she showed distinct avoidance behaviour in an effort to try to maintain a minimum of emotional stability and functionality.
Her initial childhood traumatic experiences were reactivated when an unknown person touched her from behind about two months ago. As she was worried about being unable to take appropriate care of her two children after the birth of the second one, she requested cue-exposure therapy before delivery. During a careful examination, we found that she fulfilled the criteria for cPTSD according to ICD-11 (international classification of diseases 11th revision; 1) (Maercker, Brewin, Bryant, Cloitre, Reed, et al., ; Maercker, Brewin, Bryant, Cloitre, van Ommeren, et al., ; Maercker, Hecker, Augsburger, & Kliem, ).
In ICD-11, the diagnosis of cPTSD is defined by disturbances in self-organization (DSO) by means of affective dysregulation, impulsivity and negative self-concept as well as disturbances in relationships to others in addition to the classical PTSD symptom cluster (Karatzias et al., ). In this regard, particularly overwhelming, long-lasting, reoccurring traumatic experiences during childhood, such as sexual abuse, are considered a risk factor for the development of cPTSD (de Aquino Ferreira, Queiroz Pereira, Neri Benevides, & Aguiar Melo, ).
Besides the core criteria of PTSD, DSO were seen through difficulties in appropriate regulation of trauma-related emotions such as anxiety, anger and intense feelings of helplessness, as well as an increased and impairing level of fear and irritability in social situations. The sexual relationship with her husband was severely impaired. Furthermore, the patient was burdened by her negative self-concept as a bad mother. Apart from the cPTSD diagnosis, she did not fulfil the complete criteria for any other mental disorder.
In advance of the in-patient admission to our 12-week exposure-based DBT-PTSD program (Bohus, Dyer, et al., ), her gynaecologist was consulted and an individual risk-benefit-assessment was conducted (for more details please refer to the discussion). Mrs S. started her treatment when she was pregnant during the second trimester (21st week of pregnancy). Her gynaecologist routinely observed the course of pregnancy during the whole course of the treatment without reporting any serious adverse events. Psychometric measurements Davidson Trauma Scale (DTS) and Borderline Symptom-List-23 (BSL-23) were used to observe the course of treatment regarding common PTSD-symptoms and DSO. The Davidson Trauma Scale (DTS) is a 17-Item self-rating scale with a good internal as well as retest reliability and validity, measuring PTSD symptom severity in terms of trauma-related re-experiencing, avoidance behaviour and hyperarousal (Davidson et al., ). For the single items, scores between 0 and 1 point to asymptomatic or low symptom severity, scores around 2 point to moderate symptom severity and scores between 3 and 4 to high or very high symptom severity. Further, the test retest reliability is reported to be r = 0.86. According to Davidson, Tharwani, & Connor (), the distribution in a normative general population has been found to be at mean (SD) = 11.0 (18.1).
Statistically reliable changes regarding symptom improvement over the time course of therapy were examined by means of the reliable change index (RCI) as suggested by, for example, Jacobson & Truax, (). Thus RCI was calculated using the reported test-retest reliability as well as the SD of the normative population as
whereby represented the total sum score of the DTS at the beginning of treatment (week of pregnancy 21) and represented the total sum score at the end of treatment (week of pregnancy 31). According to Jacobson, the cut-off value for RCI was set to 1.96.
The BSL-23 is also a self-rating instrument, with a range from 0 (symptoms absent) to 4 (symptoms clearly present), examining symptoms, which are typically increased in patients with Borderline personality disorder (BPD) such as emotional dysregulation, and negative thoughts and feelings about oneself and others (Bohus, Limberger, et al., ), and was therefore used to assess DSO-related impairments. For BPD patients, the average score is known to be around mean (SD) = 2 (0.76), whereas healthy controls score around mean (SD) = 0.4 (0.22). Again, the internal as well as retest reliability has been judged as high (Bohus, Limberger, et al., ). Furthermore, the change-sensitivity has been rated as highly significant (p < 0.0001) (Wolf et al., ).
To address a particular group of patients suffering from core PTSD symptoms and severe impairments of DSO, DBT-PTSD was developed (Bohus, Dyer, et al., ). This treatment option is based on the dialectical principles of standard DBT focussing on mindfulness, distress tolerance, emotion regulation and interpersonal effectiveness (Linehan et al., ). Seven treatment phases characterize DBT-PTSD (commitment, trauma-model and motivation, skills and cognitive elements, skills-assisted exposure, radical acceptance, a life worth living, and farewell) (Bohus, Dyer, ; Bohus et al., ). The essential difference between DBT-PTSD and the standard Prolonged Exposure Protocol (Harned, Korslund, Foa, & Linehan, ; Harned, Korslund, & Linehan, ), is that exposure sessions are conducted in a skills-assisted manner in order to prevent dissociative symptoms during exposure. This takes account of the finding that state dissociation during psychotherapeutic interventions is accompanied with reduced treatment outcomes (Kleindienst et al., ).
During the first treatment period (weeks 1–3), individual psychotherapeutic goals of Mrs S. were derived from a problem analysis (1. reduction of avoidance behaviour and escape strategies by means of trauma-confrontation, 2. improvement of abilities to distance herself from others, 3. improvement of sexuality) and Mrs S. learned how to use distress tolerance skills effectively to prepare herself for the exposure treatment.
During the second period (weeks 4–9), a graded exposure-based treatment started at the beginning of the 24th week of pregnancy. In our case, the skills-assisted exposure took place in two therapist-guided sessions per week followed by self-management sessions (3 sessions/week), during which the patient repeatedly listened to recordings of the therapist-guided in sensu exposure sessions. In order to prevent dissociative symptoms during self-administered exposure, the computer program Morpheus was applied. Morpheus continuously monitors the level of dissociative states and offers state-related antidissociative skills (Gorg et al., ).
In addition to exposure, Mrs S. worked on distancing herself from her mother and practiced self-care skills. The last treatment period focused on the transfer from the clinical setting to everyday life.


In 19 April 2020, a 2-month-old male infant was taken to the hospital with fever (as the sublingual temperature more than 38°C) and diarrhea. He has these symptoms for 3 days (16 April, 2020). His past medical history was unremarkable, and he ignored using any drugs, medications, or hospitalization. Because his hospitalization occurred at the time of COVID-19 crisis, the infant was suspected to have the SARS-CoV-2. Therefore, the initial diagnosis for the infant was COVID-19 confirmed after the accurate evaluation with real-time reverse-transcriptase polymerase chain reaction or rRT-PCR (based on routine PCR testing and sequencing of PCR amplifiers using throat swabs) and computed tomography (CT) scan of the chest. Dyspnea, rhinorrhea, and increased frequency of diarrhea caused the infant's condition to worsen the second day after the initial diagnosis of COVID-19 pneumonia, which was why the patient was hospitalized in the intensive care unit. The chronology of events by the parents confirmed that the patient was not infected with COVID-19 due to the history of close contact with the parent. Given that the outbreak of COVID-19 began for the first time in the city of Qom, located in the center of Iran country, his parents reported that they resided at the high-risk areas of the Qom city. Interestingly, the child's parents who had to be close enough to take care of their child, regardless of the principles of protection and distance, have negative results for the SARS-Cov-2 (negative rRT-PCR, complete blood cell; erythrocyte sedimentation rate, C-reactive protein [CRP], and chest CT scan). They reported that their young child had no close contact with the suspected or confirmed COVID-19 in the close family. The parents of the child not presented any detailed data related to way of infection for the child.
Upon admission to the hospital, he looked ill, and his vital signs were as follows: blood pressure, 85/40 mmHg; pulse rate, 140 bpm; respiratory rate, 60 bpm; and oral temperature, 38°C. Laboratory assays were as follows: white blood cell, 15.1×103; red blood cell, 3.55×106/µL; platelets, 367×103/µL; hemoglobin, 10.7 g/dL; creatinine, 0.5 mg/dL; Na, 139 mEq/L; K, 5.4 mEq/L; Ca, 9.2 mg/dL. A summary of the clinical outcomes is given in . alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase values were in normal range. At day of hospitalization, echocardiography was performed that not revealed any abnormality as the patient was stable (mild tricuspid regurgitation, pressure gradient=17 mmHg, left ventricular ejection fraction=68%, good left ventricular function, normal pulmonary artery pressure). Total protein and CRP-1h levels were in normal range and were equal to 0.3 mg/dL (reference: quantities <10 considered as negative) and 4.2 g/dL (normal range; for child between 1 month to 6 months: 4.4 to 6.6 g/dL) (). In blood culture test, we did not find any bacteria growth after 72-hour incubation of the blood sample. After the initial diagnosis of COVID-19, the chest CT scan was performed as revealed bilateral lung involvement with pleural effusion and pneumothorax in right lobe ().
At the course of the disease, the SpO2 reduction was not seen for the patient. Due to the young age of the patient, we started medication with hydroxychloroquine (3–5 mg/kg/day twice daily) and lopinavir/ritonavir (3 mg/kg/dose, twice daily) after medical consultation with pediatricians in our department (similar treatment as algorithmic approach was proposed to management of children with severe 2019-nCoV pneumonia or those with underlying diseases) []. After 5 days of medication, the patient was discharged from the hospital with partial recovery (at the day of discharge, the patient still had mild diarrhea without fever). In the follow-up in which we performed a week after the patient's discharge from the hospital, the patient was completely recovered and all the initial symptoms were subsided. The follow-up for pneumonia was done by chest radiography and evaluation of the clinical symptoms. After the beginning of the treatment, we follow up the patient in duration of 4–6 weeks via chest radiography. After treatment, when the patient recovered, chest radiography was normal. Also, we did not find any evidence of crackle auscultation in the patient. After treatment and recovery, the patient did not show any clinical symptoms associated with pneumonia, including fever, dyspnea, and cough. For pneumothorax, the follow-up was performed within 12–24 hours, as decreasing of auscultation was not seen. Also, chest radiography was clear for the patient. After 1-week treatment, we do not find any clinical symptom related to pneumothorax in the patient such as dyspnea.
Approval was obtained from the ethics committee of Qom University of Medical Sciences. The procedures used in this study adhere to the tenets of the Declaration of Helsinki (Nu: IR.MUQ.REC.1399.056).


A 52-year-old female with hypertension, type 1 diabetes mellitus, Hashimoto’s thyroiditis, and pernicious anemia, under the umbrella diagnosis of PGAS type II, was referred to Dermatology for evaluation of asymptomatic hyperpigmentation of the palms, soles, hard palate, and tongue for 6 months ( and ()). Dermoscopy was not performed on the mucocutaneous lesions. The patient denied personal or family history of irregular hyperpigmentation and denied any itching or pain associated with the lesions. Review of systems was notable for fatigue, without associated fevers, chills, joint pain, swelling, numbness, or sensory loss. Medications prior to onset of hyperpigmentation included long-acting insulin, atorvastatin, and iron supplementation. Initial differential included Laugier–Hunziker syndrome, Addison’s disease, Peutz–Jeghers syndrome, or an acquired or drug-induced nutritional deficiency.
Laboratory investigations demonstrated a chronic macrocytic anemia with pancytopenia, with an unremarkable infectious work-up. Hemoglobin on admission was 5.6 g/dL (12.0–15.5 g/dL), which decreased from a baseline of 10.7 g/dL with lactate dehydrogenase (LDH) elevation to 1669 U/L (normal <280 U/L), and peripheral blood smear revealed hemolysis. Following transfusion, the patient underwent endoscopy showing antral mucosal glandular hyperplasia and atypia, as well as gastric nodules. Anemia work-up confirmed vitamin B12 deficiency, that is, <50 pg/mL (normal, 190–900 pg/mL). In addition, homocysteine and methylmalonic acid (MMA) levels were elevated to 113.3 µmol/L (normal, <15 µmol/L) and 38.980 µmol/L (normal, 0.00–0.40 µmol/L), respectively, with confirmation of serum intrinsic factor and parietal cell antibodies. This led to the diagnosis of pernicious anemia secondary to vitamin B12 deficiency. The patient was initiated 1000 µg of vitamin B12 intramuscular injections daily for 1 week with transition to maintenance oral therapy for 6 months. At that time, her B12 level increased to 844 pg/mL, and there was significant improvement in hyperpigmentation ( and ()).


Patient is currently an 18-year-old male who had initially presented with HA, lethargy and respiratory distress at 30 hours of life. Subsequent biochemical (undetectable citrulline and elevated glutamine with orotic aciduria) and genetic testing (pathogenic variant in exon 9 of OTC gene) confirmed a diagnosis of OTC deficiency. Treatment was started with oral ammonia scavengers and protein restricted diet. His clinical course remained relatively well controlled without any known hyperammonemic crisis. He did develop seizure disorder for which he was continued on levetiracetam. He had mild developmental challenges as a child and was also diagnosed with attention deficit hyperactivity disorder at 8 years of age.
In the admission pertaining to our study, he presented with acute alteration in mental status after a few days of upper respiratory symptoms. Ammonia level at presentation at an outside facility was greater than 400 millimoles/L. Therapy was initiated with intravenous sodium benzoate and sodium phenylbutyrate infusion. He was also started on fluids containing 10% dextrose and intralipids. There was no other evidence of metabolic perturbations at transfer such as hypoglycemia, metabolic acidosis or liver dysfunction. Plasma amino acid profile showed glutamine to be raised at 627 millimoles/L. After 2 days of intravenous ammonia scavenger therapy, patient’s mentation improved significantly and ammonia level was trending down. He then started experiencing dysarthria and dysphagia. Etiology of these symptoms was attributed to post-influenza encephalitis based on CSF studies. Treatment was attempted with intravenous methylprednisone and immunoglobulin. There was a steep rise in ammonia level (up to 229 millimoles/L) after starting him on methylprednsione. Steroid treatment was discontinued and sodium benzoate and sodium phenylbutyrate were restarted. Ammonia level stabilized eventually and once he was at his neurological baseline, he was transferred to a rehabilitation center.


A 61-year-old male patient, biopsy-proven case of moderately differentiated colorectal adenocarcinoma, referred for 18F fluorodeoxyglucose positron emission tomography–computed tomography (18F-FDG PET-CT) scan for staging. PET-CT scan was done on SIEMENS Biograph TruePoint 16-slice CT scanner after 60 min of 370 MBq 18F-FDG intravenous injection.
The scan revealed high-grade FDG-avid enhancing asymmetric circumferential wall thickening of 14 mm involving distal sigmoid colon, rectosigmoid junction, and proximal rectum with length of involved segment –80 mm and FDG avid multiple locoregional sigmoid mesenteric and mesorectal lymph nodes []. The scan also revealed high-grade FDG-avid (maximum standardized uptake value [SUVmax] 12.9) mild enhancing portal vein thrombus extending into the right main branch and left main and segmental branches with ill-marginated wedge-shaped hypodense areas in segment IV representing parenchymal involvement [Figures and ].
The patient has received 4 cycles of chemotherapy and referred for FDG PET-CT scan for response evaluation [], and follow-up scan revealed significant reduction in metabolic activity and malignant wall thickening of distal colon and good response in locoregional nodes []. Follow-up scan also revealed complete resolution of hepatic parenchymal lesion and complete metabolic resolution (CMR) of PVTT []. However, thrombosis was further extended into entire length of superior mesenteric vein (SMV) and part of splenic vein with development of multiple collaterals in periportal and peripancreatic head region which suggested portal vein cavernoma formation []. There was also development of mild ascites [], congested small bowel mesentery, and stranding in greater omentum which is suggestive of mesenteric ischemia [].


A 55-year-old female with a medical history significant for well-controlled diabetes mellitus complicated by proteinuria presented for a follow-up visit. On this visit, she reported shortness of breath, weight gain of 5.5 kg, and lower extremity swelling. She denied any new over-the-counter medications usage, hemoptysis or hematuria, sore throat, rash, or fever. Her glycemic control was fair on oral hypoglycemics. Her outpatient medications included baby aspirin, losartan, metformin, zinc. Other past medical history included hypertension, morbid obesity, vitamin D deficiency, and history of tobacco abuse. She used to smoke one pack per day but quit a little over a year ago. The patient's proteinuria significantly changed, and microalbumin to creatinine ratio was 5.5 g, which is considerably worse than her baseline of less than 500 mg.
Her vital signs were recorded as temperature of 36.8°C, pulse 84/min, blood pressure 138/78 mm Hg, respiratory rate 16/min. On examination, her chest was clear to auscultation, and no rubs, murmurs or gallops were noted. Pedal edema was present. Her labs were significant for microalbumin to creatinine ratio, which was elevated to 9,155 on repeat testing. Her microalbumin to creatinine ratio was less than 0.5 gms 4 months ago. Albumin dropped to 3.2 mg/dL, and it was within normal range 4 months ago. Her urine analysis showed proteinuria and blood (Table ). Her creatinine was 0.9 mg/dL (at baseline) and Bun 17 mg/dL. Due to the acute onset of nephrotic range proteinuria, kidney biopsy and serological workup were planned to find the exact etiology.
She was admitted to the hospital for CT-guided renal biopsy, and extensive serological workup was ordered. Her serum protein electrophoresis (SPEP) did not show monoclonal bands. She had a mild elevation of kappa light chains, but the kappa/lambda ratio came back as normal (1.23). She tested negative for HIV, cryoglobulins, hepatitis B and C. Her C3, C4, beta-2-microglobulin were within the normal range (Table ). Her antibodies, including antinuclear antibody (ANA), proteinase antibody (PR-3), myeloperoxidase antibody (MPO), glomerular basement membrane (GBM) antibody, were negative.
The renal biopsy sample was processed according to the standard techniques. Multiple sections were stained with hematoxylin and eosin (HE), periodic-acid Schiff's (PAS), John methenamine silver (JMS), and trichrome stain. The biopsy specimen showed the renal cortex containing 16–28 glomeruli per level section, of which one (5%) was globally sclerosed. Approximately 50% of the glomeruli showed segmental mesangial and endocapillary hypercellularity due to cellular proliferation and influx of leukocytes, with many polymorphonuclear leukocytes (Fig. ). At least two glomeruli showed small cellular crescents (Fig. ) and at least two other showed segmental adhesions of glomerular tufts to the adjacent Bowman's capsules. The glomerular capillary walls were irregularly thickened with focal “spikes” of the basement membrane, segmental membrane vacuolization, or double focal contour (Fig. ). Mild patchy interstitial fibrosis and tubular atrophy were noted (approximately 7%). Occasional tubular segments contained red blood cells. Arteries and arterioles were without significant sclerosis or evidence of vasculitis. Staining with Congo red reagent for amyloid was negative.
Immunofluorescence microscopy showed granular, predominantly capillary wall staining for IgG(ab) and IgGw (both 1–2+), C3 (2+), kappa (trace to 1+). There was no significant glomerular staining for IgA, IgM, C1q, lambda light chains, fibrinogen, or albumin. There was no staining of the tubular basement membranes, interstitium, or vessels for any of the tested immune reactants. Analysis of IgG subclasses demonstrated a polyclonal staining pattern with antisera specific for IgG1 (2+), IgG2 (2+), and IgG4 (trace). Staining for IgG3 was negative.
Ultrastructural examination revealed numerous subepithelial and intramembranous immune type deposits. Many of the deposits were separated or surrounded by basement membrane-like-material. There was a frequent remodeling of capillary walls with focal duplication and cellular interposition. Occasional small mesangial and sub-endothelial deposits were also identified. The immune deposits were organized into randomly arranged, nonbranching fibrils measuring, on average 13.3 nm (range from 9.9 to 18.2 nm) in thickness (Fig. ). The fibrils were somewhat rod-like, focally hollowed, and/or have cross-striations (with ladder-like appearance). The glomerular epithelial cells (podocytes) showed extensive effacement of foot processes. Many of the capillary loops contained circulating leukocytes, which focally encroached upon the capillary basement membrane causing significant thinning. Tubuloreticular inclusions were not seen in the endothelial or other cell types. No evidence of immune deposits was seen in the tubular basement membranes or the interstitium. Tubular cells contained lipid droplets.
Given the small fibrils size and negative staining for Congo red, the initial impression was fibrillary glomerulonephritis. However, additional staining for DNAJB9 (that is 98% sensitive and >99% specific for the diagnosis of fibrillary glomerulonephritis) was found to be negative.
The final diagnosis was acute proliferative glomerulonephritis with an atypical pattern of organized IgG immunoglobulins. Bone marrow biopsy performed as a part of secondary workup following the results of kidney biopsy showed normocellular bone marrow with 40% cellularity with trilineage hematopoiesis and less than 5% blasts. No evidence of myelodysplasia, lymphoproliferative disorder or plasma cell dyscrasia was noted. Fluorescence in situ hybridization (FISH) for multiple myeloma panel was found within normal limits. Cytogenetics did not suggest any abnormalities. Flow cytometry results did not suggest any definitive evidence of myeloid dysplasia, lymphoproliferative, or plasma cell dyscrasia. On clinical follow-up, the patient was initially treated with pulse steroids and subsequently received two doses of rituximab, 1 g each, 2 weeks apart. At follow-up, proteinuria dropped to the sub-nephrotic range with a resolution of edema and improvement in serum albumin. Her GFR has remained stable.


A 19-year-old male patient visited our emergency department due to severe right-sided headache and nausea without significant neurologic deficit. He was admitted to the neurology ward under the impression of intracranial insults. Bacterial culture and Indian ink stain for Cryptococcus were negative in cerebrospinal fluid. Therefore, acyclovir and ceftriaxone were discontinued 1 week later. Elevated microalbumin (88.57 mg/dL, normal range 10–30 mg/dL) and total protein (61.9 and 139.1 mg/dL, normal range 15–45 mg/dL) were detected in two series of cerebrospinal fluid studies with a 1-week interval. Serum vitamin B12 was relatively low (138 pg/mL, normal range 180–914 pg/mL). Electroencephalography did not detect cortical dysfunction. The results of magnetic resonance imaging and computed tomography studies were nonsignificant. He was discharged with a vitamin B12 supplement. One week after discharge, although headache had improved, he experienced neck stiffness and pain which later evolved with intermittent involuntary movement in his throat, mouth, and tongue as well as right lateroanterior torticollis (Fig. ). The patient walked independently without device into the physical medicine and rehabilitation outpatient clinic 2 months after seeing several doctors for his discomfort. Upon examination, his neck was tilted to the right and forward with tight sternocleidomastoid, trapezius, splenius capitis, and levator scapulae muscles. Intermittent slow jaw opening and tongue protrusion with rapid up and down movement of both ears were noted. In neurologic examination, there were a positive Romberg test with abnormal tandem and a positive reverse tandem walk test. The finger-nose-finger test did not show dysmetria. Sitting and standing static and dynamic balance were good. The patient did not have difficulty in activities of daily living and had no difficulty in using chopsticks for taking meals. However, his social and occupational participation as a university student were interfered due to body image disfigurement. He was treated under the impression of oropharyngeal and cervical dystonia. The patient was referred back to a neurologist, but he had poor compliance to prescribed medications.
Therapeutic modalities including transcutaneous electrical nerve stimulation and hot packing did not improve his neck pain and tightness. He also complained of painful swallowing and engorgement in his throat, with occasional nausea when eating. Although he had no deterioration in articulation, phonation, or loudness, he could only speak in short sentences during intervals of dystonia remission. A significant reduction in body weight (10 kg) within 3 months was mentioned by the patient, and dry skin and lips were observed as signs of malnutrition and dehydration. For the swallowing difficulty, videofluoroscopic swallowing study revealed inefficient bolus formation due to repetitive tongue movement, premature leakage, and mild vallecula stasis without penetration or aspiration (Fig. ). Our speech-language pathologist taught him safe swallowing techniques like repetitive swallowing and throat clearance, and compensatory swallowing technique like taking meals with thick consistency and food with no need for much chewing, and separated meals in decreased amount. Dystonia and its consequential symptoms improved spontaneously 6 months after onset since the patient did not take the prescribed medication. Fortunately, dysphagia-related aspiration pneumonia did not occur throughout the clinical course in this patient.
He was also referred to a psychiatrist due to lots of somatic complaints and anxious state. Since the criteria of depression, anxiety, or mania were not met, we referred this patient to a social worker for suggesting resources from his family, school, and community for emotional support. His anxious state was relieved along with clinical improvements. His doctor shopping also stopped since symptom relief. He then resumed his social and occupational activities as a university student.


A 30-year-old Tunisian man has presented to Hamad General Hospital, a tertiary hospital in the state of Qatar, with severe left flank pain associated with headache. The patient was sweating, anxious, and in excruciating pain. He reported diffuse left-sided chest pain and shortness of breath. He denies fever, vomiting, diarrhoea, trauma, haematuria or any urinary manifestation. He had an episode of chest pain 1 month ago for which he was treated in another hospital as non-ST segment elevation myocardial infarction. The patient was married without children and a nonsmoker. The patient gave a history of high blood pressure a few months ago when his general practitioner started him on amlodipine 5 mg, which he used for a week and stopped with no follow-up. The patient had no known allergies.
The physical examination yielding that his blood pressure was 162/102 mm Hg, his monitored heart rate was 116 bpm, his respiratory rate was 21 per minute, his oxygen saturation was 98%, and he was afebrile.
He was fully conscious and had no neurological deficit. Chest and heart examination were unremarkable. The abdomen was distended with tenderness on the left side. His extremities examination showed equal bilateral peripheral pulses with no signs of deep vein thrombosis.
Bedside point-of-care ultrasound (POCUS) showed no hydronephrosis bilaterally, no free fluids, a normal diameter of the aorta. The heart has normal contractility, no right-sided strain and had no pericardial effusion.


The 2-year-old male child was consulted by our department with a prediagnosis of RS. He was born as the third child of the family by cesarean section at the 38th gestational week with a birth weight of 2050 g (3rd percentile). He had jaundice, which started on the postnatal 5th day. Dysmorphic examination performed after excluding other diseases that cause hemolysis revealed no findings except for a mild icteric appearance. His height and weight were found at the 50–75th percentile. Laboratory findings were as follows: aspartate aminotransferase (AST): 32 U/L (5–34 U/L), alanine aminotransferase ALT: 18 U/L (0–55 U/L), gamma-glutamyl transpeptidase (GGT): 15 U/L (12–64 U/L), alkaline phosphatase (ALP): 124 U/L (40–150 U/L), total bilirubin: 2.53 mg/dL (0.2–1 mg/dL), and direct bilirubin: 1.77 mg/dL (0–0.5 mg/dL). Whole abdominal ultrasonography revealed no pathologic findings. Chromosomal microarray analysis was performed on a DNA sample obtained from peripheral blood using an Affymetrix CytoScan Optima (315k) device (Thermo Fisher, MA, USA). All data were analyzed using the ChAS 3.1 program (Thermo Fisher, MA, USA). A homozygous deletion of 340 kilobase (kb) was observed in the short arm of the 12th chromosome on microarray analysis: arr[hg19] 12p12.2p12.1 (21,017,795–21,357,948)x0. This region involved the first 10 exons of SLCO1B1 and the final eight exons of SLCO1B3.


A 23-year-old woman visited our otorhinolaryngology clinic with symptoms of aural
fullness in the right ear for several months. She had no history of repeated cold water
irritation to the ear. On physical examination, an ovoid hard mass was observed in the
right EAC (). Temporal
bone computed tomography revealed a 0.5 cm × 0.5 cm anterior-based, pedunculated, bony
mass originating from the tympanosquamous suture line (). Because the tumor was of bone origin,
surgical excision was planned.
With microscope assistance, the mass was surgically excised at the level of the peduncle
via transcanal approach with the patient under local anesthesia. The pedunculated mass was
broken easily with curette and alligator forceps. The base of the excised mass was drilled
with a diamond burr to further remove all osseous lesions. The tympanic membrane was
intact and there were no other lesions such as cholesteatoma medial to the excised
osteoma. After excision, skin graft was not necessary because the skin defect was minimal,
and the EAC was packed with gelfoam.
Histopathologic findings showed lamellated bone covered with stratified squamous
epithelium with a variable amount of fibrofatty marrow tissue, consistent with spongiotic
osteoma (). Two years
and eight months after surgery, the patient is without symptoms and has not experienced
any tumor recurrence.


A 19-year-old man visited our otorhinolaryngology clinic with a known mass in the right
EAC. He had reported mild symptoms with aural fullness for several years. On physical
examination, an ovoid hard mass was observed in the right EAC (). Temporal bone computed tomography
revealed a 0.6 cm × 0.5 cm anterior-based, pedunculated, bony mass originating from the
tympanosquamous suture line (). Because the tumor was of bone origin, surgical excision was planned.
As in Case 1, surgery was performed, and pathology revealed a spongiotic osteoma (). Two years and five
months after surgery, the patient is without symptoms and there has been no tumor
recurrence.


A 44-year-old man with right vocal cord palsy and recurrent aspiration was admitted to the intensive care unit (ICU) for respiratory failure due to carbapenem-resistant Acinetobacter baumannii pneumonia. He was put on mechanical ventilator support and the ventilator (Servo-U, Maquet) was connected to a scavenging system (EVAC 180) as an additional infection control measure in face of the COVID-19 epidemic. On the fifth ICU day, the heat moisture exchange (HME) in the breathing circuit was changed to a heated humidifier (Fisher and Paykel MR850) due to copious amount of sputum. On the sixth ICU day, his condition continued to improve and he was on PS mode with PS of 10 cmH2O above a PEEP of 6 cmH2O. Twenty-eight hours after he was put on PS mode, he became dyssynchronous with the ventilator, and labored breathing was observed. Despite the patient's respiratory effort, the backup pressure control (PC) was activated with a backup mandatory breath rate of 15 breaths/minute (bpm). Despite low inspiratory flow being delivered at a rate of 15 bpm, neither triggered nor mandatory breath could be recorded (). Paradoxical changes in airway pressures were observed with a decrease in pressure from 28 to 20 cmH2O during the inspiratory phase and an increase in pressure from 20 to 28 cmH2O during the expiratory phase. The ventilator wrongly regarded the expiratory pressure of 28 cmH2O as peak pressure and the inspiratory pressure of 20 cmH2O as PEEP. Ten to 20 seconds afterward, PS breaths were seen to be superimposed on a similar pattern of paradoxical pressure changes. Specifically, PS breaths of 10 cmH2O (with airway pressure up to 17 cmH2O) were triggered by flow when the airway pressure dropped below 8 cmH2O (). End-tidal CO2 (ETCO2) varied between 75 and 90 mm Hg. It was also noted the reservoir bag of the scavenging system was hyperinflated () and water condensate was seen in the tubing connecting the ventilator exhaust outlet and the scavenging system. The reservoir bag was removed for inspection and was found filled with water condensate. Patient-ventilator dyssynchrony was abolished immediately after the water condensate was drained (). Such an event did not recur when the emptied reservoir bag was reinstalled into the scavenging system ().
The patient was weaned and extubated on the 8th ICU day. On the 15th ICU day, he developed right pneumothorax for which did not require drainage. He underwent further rehabilitation and was discharged from ICU after 29 days.


We describe the case of a female patient, 47 years old, born in Brazil and living in Portugal for 12 years, with a personal history of vaginal uterine myomectomy in 2012, polycystic ovary disease and medicated with an anticonception pill, and a family history of unspecified thyroid pathology (sister) and unspecified parathyroid pathology (father), without other relevant family history.
The patient underwent mammography in December 2013 after self-detection of a nodule in the left upper-inner breast quadrant, which documented a suspected nodular lesion in that location. She was referred to a Breast Surgery consultation, presenting a palpable firm lesion in the left upper-inner quadrant, about 3×2 cm, with irregular borders and hard consistency, adherent to the deeper planes—without palpable adenopathies and without other relevant findings. In February 2014, an ultrasound-guided biopsy of the referred lesion was performed, which revealed invasive ductal carcinoma (no special type (NST)), grade 2 of histological malignancy, with the following molecular profile: oestrogen receptors, 100%; progesterone receptors, 100%; Ki67, >20%; p53 negative; and the absence of amplification of the HER2 gene (luminal B). A breast MRI was performed for locoregional staging, which confirmed, in T1 weighting, the presence of a lesion with irregular nodular morphology, with heterogeneous contrast uptake, 30×25 mm in dimension, without evidence of multifocality, multicentricity or nodal disease. No pathological changes were detected in the contralateral breast by any of these imaging tests ().
After discussion of the case by a multidisciplinary team, it was decided to perform a sentinel lymph node biopsy followed by neoadjuvant chemotherapy. Sentinel node biopsy was performed in March 2014, which did not document the presence of neoplastic tissue.
Clinical staging was completed with thoraco-abdominal-pelvic CT scan with administration of oral and intravenous contrast in April 2014, which identified in the upper lobe of the right lung a 10 mm non-calcified hypodense solid nodule (of undetermined nature by this examination), heterogeneous uterus and increased dimensions of both ovaries, with hypodense parenchyma. There was no evidence of nodal or metastatic disease. This study was complemented with abdominal and pelvic ultrasound (suprapubic and endocavitary), which revealed three myomatous formations in the uterus (two subserous and one submucosal) and ovaries with increased dimensions (with 4.1 cm of greater axis on the right and 3.6 cm of greater axis on the left), with several millimetric follicles, without other major changes. It should be noted that at this time none of the tests revealed pathological changes in the pancreas.
Regarding the nodule of the upper lobe of the right lung identified by CT imaging, a CT-guided needle aspiration biopsy was performed, whose histopathological analysis revealed aspects compatible with a carcinoid tumour (positive for thyroid transcription factor 1, chromogranin A, synaptophysin and CD56) ().
Laboratory evaluation showed no elevation of tumour markers (carcinoembryonic antigen (CEA) and cancer antigen (CA) 15-3)), but demonstrated a persistent elevation in calcium (12.3 mg/dL; normal reference value: 9–10.5 mg/dL); the parathyroid hormone (PTH) level was 478 pg/mL (normal reference value: 14–72 pg/mL), without increased vitamin D value and without hypoalbuminaemia. Of the remaining laboratory results, we highlight the following: serum phosphorus, 2.1 mg/dL; thyroid-stimulating hormone, 0.97; fT3 (free tri-iodothyronine) and fT4 (free thyroxine) within normal values; negative antithyroid antibodies; and calcitonin, prolactin, adrenocorticotropic hormone, serum cortisol, urinary cortisol, insulin-like growth factor 1 (IGF-1) and urinary catecholamine assay all within normal reference values.
A cervical ultrasound was requested, which showed, below the left lobe of the thyroid, the presence of a 23×12 mm hypoechoic solid oval lesion with a probable origin in the parathyroid gland. This study was complemented with parathyroid scintigraphy, which confirmed the suspicion of left parathyroid adenoma ().
Thus, the patient had three distinct pathological entities—invasive carcinoma of the left breast (cT3N0M0), carcinoid tumour of the right lung and primary hyperparathyroidism. After completing six cycles of neoadjuvant chemotherapy (four cycles of adriamycin and two cycles of paclitaxel; completed in July 2014), with an imagiological response greater than 50% in breast MRI, she underwent tumorectomy+contralateral mammoplasty in August 2014. The histopathological analysis of the tumorectomy specimen confirmed a ductal invasive carcinoma of the breast, with 1 cm major axis, with tumour-free surgical margins. Adjuvant radiotherapy was performed to the left breast with a boost over the tumour bed (total of 60 Gy in 30 fractions), and the patient was given maintenance therapy with tamoxifen ().
In October 2014, an atypical resection of the right lung was performed, whose histopathological analysis of the surgical specimen confirmed a typical carcinoid tumour, with a Ki67 of 2% ().
A left lower parathyroidectomy was performed in November 2014, with the analysis to the surgical specimen confirming the suspicion of parathyroid adenoma ().
There were no postoperative complications related to the surgeries described above. The patient was followed up in a General Surgery, Oncology and Endocrinology consultation, revealing improved levels of calcium and PTH.
In 2016, a follow-up CT scan detected a 1.6×1.3 cm biloculated cystic formation in the pancreatic tail, with peripheral contrast uptake (). A laparoscopic enucleation of the lesion was performed, without complications. The histopathological analysis of the specimen documented a NET (positivity for chromogranin and synaptophysin) of 1.9 cm of major axis, grade 1 of malignancy, with Ki67 below 2%, without images of lymphoangioinvasion and with free surgical margins.
Because of the presentation of multiple neoplastic lesions whose set fit the spectrum of the MEN-1 syndrome in this patient, she was referred to a Medical Genetics consultation, and a genetic study was carried out—an analysis of a peripheral blood DNA sample was performed by ‘new-generation’ sequencing (next-generation sequencing) using the TruSight Cancer Gene Set methodology. Molecular analysis of the MEN1 and HRPT2 genes was performed; research was also carried out on major deletions/duplications of the MEN1 gene using the multiple ligation-dependent probe amplification technique. A germline heterozygote mutation was detected, c.249_252delGTCT, in exon 2 of the MEN1 gene, which encodes a truncated protein (p.Ile85SerfsX33)—this mutation consists of a 4 bp deletion starting at codon 85; the in silico analysis carried out with the Mutation Taster software classified this variant as causing disease, and the Human Genome Database classifies it as pathogenic; this mutation is one of the most frequent in families with MEN-1; this result was compatible with the diagnosis of MEN-1 syndrome.
The patient maintained follow-up with General Surgery, Oncology and Endocrinology. No tumour recurrence or metastatic disease of breast carcinoma, lung carcinoid tumour or NET of the tail of the pancreas was observed during the follow-up period (6 and 4 years, respectively).
Due to recurrence of primary hyperparathyroidism associated with a hypoechoic solid nodule of 12×10 mm in the right lobe of the thyroid (with aspiration cytology compatible with follicular tumour), the patient underwent another surgical procedure in May 2018—right thyroid lobectomy+right lower parathyroidectomy, revealing intraparenchymal parathyroid with hyperplasia/adenoma (corresponding to the nodule described in cervical ultrasound) and hyperplasia of the right lower parathyroid in the surgical specimen, without thyroid neoplasia tissue ().
The patient has kept follow-up by the previously mentioned specialties, presenting at the moment without evidence of recurrent or de novo neoplastic disease. There were no complications related to any of the surgeries performed. A normalisation of the levels of calcium and PTH has been observed after the last surgery performed, and no elevation of tumour markers (CEA, CA 19.9 and CA 15-3) or other pathological parameters has been documented to date.


A 54-year-old man presented with a three-year history of pain and tingling sensation on the anterolateral side of his left thigh. Symptoms were increased while standing and walking. Pregabalin was started and gradually increased to 450 mg/day one year ago, and complaints were reported to decrease. However, for the last one month, symptoms were aggravated. There was no sign of chronic disease in his past medical history. The range of motion of the lumbar and bilateral hip, muscle strength and deep tendon reflexes of both lower extremities were found to be normal upon physical examination. Lateral pelvic compression test results were positive. The Tinel’s sign around the ASIS was negative. Erythrocyte sedimentation rate (ESR) was slightly increased (23 mm/h), whereas other laboratory test results were found to be within the normal range. Magnetic resonance imaging of lumbar and coxa-femoral joints did not reveal other possible causes of the symptoms. A solid heterogenic lesion which caused the compression of LFCN was noticed during the ultrasonographic examination (Figure 1). It was painful with sonopalpation. The LFCN was found to be thickened, compared to the right side (Figure 2). The patient was consulted to the radiology department, and the lesion was considered a reactive lymph node. Ultrasound-guided LFCN block with 1 mL betamethasone and 4 mL 0.5% bupivacaine was performed, and immediately after the injection, the pain level decreased from 8 to 3 using the numeric rating scale (NRS). A pruritic lesion at his left thumb was noticed during the detailed examination for the infectious state, and the patient was consulted to the dermatology department. Combination of oral and topical anti-fungal therapy was started with the diagnosis of tinea pedis. One month later, the patient’s pain level decreased to 1, and ESR was found to be within normal values (7 mm/h). The reactive lymph nodes were found to be smaller in ultrasonographic evaluation. At the third month, tinea pedis infection was entirely resolved, and the pain level of the patient was 0. Pregabalin dosage was gradually decreased and discontinued. The complete response to pain level remained unchanged at the sixth-month control. A written informed consent was obtained from the patient.


A 26-year-old male student had accidental acute inhalation exposure to a large quantity of titanium ethanolate and hydrogen chloride while mixing titanium chloride with ethanol. According to his record, at the time of mixing, a thick white vapor suddenly came out of the solution and he was exposed to a large quantity of the vapor for two hours. His symptoms began 3–4 hrs post-exposure. He did not get better and was referred to the emergency department of Loghman Hakim Hospital, Tehran, Iran,24 hrs after the exposure.
On arrival, the patient complained of low-grade fever, dyspnea, headache, fatigue, and myalgia. He had blood pressure of 100/70 mmHg, respiratory rate of 20/min, pulse rate of 80/min, oral temperature of 38 °C. Other vital signs were normal. Chest x-ray and physical examination of the lungs were normal. Routine lab tests were normal; there was only a slight increase in serum alanine transaminase (ALT).
After 24 hrs of symptomatic treatment with oxygen and intravenous acetaminophen (1000 mg in 200 mL normal saline),the fever was subsided, respiratory symptoms were alleviated, and the patient discharged home in a good clinical condition.


A 66-year-old male with history of hypertension, diabetes mellitus and renal transplant presented to the emergency department with several months of left hand swelling and pain. He denied any recent trauma or animal bites to his hand or arm.
On physical examination, he was afebrile with normal vital signs. The fingers of his left hand were held in moderate flexion. He had swelling and tenderness of the volar distal forearm, hand and fingers, with pain on active and passive finger extension. No erythema and warmth were present. Sensation was intact with the exception of paresthesias of the distal fifth finger. Radial and ulnar pulses were intact.
Laboratory evaluation was notable for the absence of leukocytosis (white blood cell count 5.5 × 109/L) although C-reactive protein was elevated at 14.5 mg/L. Hand radiographs were unremarkable. A POCUS was performed using a high-frequency linear-array transducer on a Zonare ultrasound system (Zonare Medical Systems, Inc., Mountain View, CA) which demonstrated a large complex fluid collection surrounding the flexor tendons of the left mid-forearm extending to the volar aspect of the left hand (). Fluid was also noted surrounding the flexor tendons of the left index finger ().
Following plastic surgery consultation, the patient was taken to the operating room for exploration, drainage and release of the left carpal tunnel. Operative findings included an extensive cavity of tenacious yellow/clear fluid with solid components extending from the left volar forearm through the carpal tunnel to the palm and volar thumb ().
Blood, fluid and tissue cultures were sent, including gram-positive, gram-negative, acid-fast bacilli (AFB) and fungal assays. The patient was empirically started on IV vancomycin, cefepime and fluconazole.
All initial cultures were negative, and preliminary AFB smear was negative. Three weeks later, wound culture results were positive for Mycobacterium avium complex (MAC). Further patient evaluation revealed the presence of a peripheral lung nodule with nodularity and cavitary changes concerning for atypical mycobacterial infection. The patient’s clinical course was complicated by the need for further operative debridement for residual MAC disease 5 months later. He was discharged on a 6- to 12-month course of azithromycin, rifabutin and ethambutol, as well as hand therapy.


A 36-year-old man with a history of traumatic brain injury, followed by depression and maintenance therapy with antidepressant drugs but without other relevant medical history, presented to our emergency department after a few days of experiencing shortness of breath, fever, and cough. Physical examination initially revealed hypotension (blood pressure 96/65 mmHg), tachycardia (heart rate 116 beats per minute), tachypnoea (respiratory rate 29 breaths per minute), impaired oxygenation (oxygen saturation 84% on room air), hyperglycaemia (blood glucose 375 mg/dL), and fever (temperature 38.6°C). The patient was immediately started on supportive oxygen via mask, and his saturation increased to 95% on 6 L of oxygen. On general examination, the patient was conscious and oriented (Glasgow Coma Score 15) and appeared tired and unwell, without other significant physical findings. By Day 5, the clinical condition of the patient had not improved markedly, and his clinical picture and laboratory values began to worsen, with sinus tachycardia (164 beats per minute), tachypnoea (respiratory rate 30 breaths per minute), fever (temperature 38°C), and his oxygen saturation remained 95% on room air.


A 49-year-old man with a history of a renal transplant eight years prior on tacrolimus and mycophenolate mofetil presented for management of a biopsy proven squamous cell carcinoma on the right temple. Mohs micrographic surgery was performed. The malignancy was cleared in three stages and the post-operative size was 1.8 cm x 1.4 cm (). The defect was closed primarily in a complex layered fashion (). A standard dressing was applied, and the patient received wound care instructions.
Two days following surgery, the patient returned to the dermatology clinic with severe pain and mild swelling surrounding his surgical site (). He denied drainage from the incision, sensation of pressure, vision changes, pain with eye movement, or systemic symptoms such as subjective fever or chills. On exam, the patient was afebrile. He had mild swelling and blanching erythema surrounding the surgical site. Tenderness to palpation was noted. No warmth, fluctuance or crepitus was observed.
Although the patient’s clinical exam was relatively unimpressive, his rapid symptom progression and severe pain were concerning for an aggressive streptococcal soft tissue infection requiring intravenous antibiotics. Labs and imaging were ordered. ENT was consulted should surgical intervention become necessary. The patient was transferred to the emergency department then admitted to internal medicine. Broadspectrum intravenous antibiotics were started including linezolid for Methicillin- Resistant Staphylococcus Aureus (MRSA) coverage (the patient reported vancomycin allergy), ceftriaxone, and metronidazole. Laboratory studies revealed a mild leukocytosis (12,500 WBCs). Two blood cultures showed no growth. A CT maxillofacial without contrast (due to the patient’s renal transplant) confirmed extensive right periorbital, cheek, and scalp tissue swelling suspicious for cellulitis. No drainable fluid collection, hematoma or abscess formation was noted.
On inpatient day two, the patient’s symptoms improved. Ophthalmology, consulted due to concern for orbital cellulitis, determined that the patient more likely had periorbital cellulitis. ENT determined debridement was unnecessary. Infectious Disease evaluated the patient and suspected a streptococcal infection due to the rapidity of onset after Mohs surgery. As the responsible organism was likely skin-derived, antibiotics were narrowed to IV Linezolid alone for gram-positive and MRSA coverage. Prior to discharge, a small amount of thin, cloudy fluid was expressed from the suture line and sent for gram stain and culture. Rare to few gram-positive cocci in pairs were seen and a moderate amount of Methicillin-Sensitive Staphylococcus Aureus (MSSA) was isolated.
On the day of discharge, the patient noted significantly decreased surgical site pain and erythema. He was discharged to complete a ten-day course of oral Linezolid ().


An 80-year-old male patient with known diabetes mellitus and essential hypertension presented with a stroke (bilateral thalamic, left occipital, and brain stem), which left him quadriplegic, bedridden, and dysphagic. To support nutrition, nasogastric tube feeding was initiated and continued for 3 weeks. There was no improvement in his dysphagia and a prolonged need for nutrition was recognized. A decision to insert a PEG tube was taken at a joint multidisciplinary meeting of the nutritionist, gastroenterologist, and primary team physician.
A 20-Fr (6.7-mm) tube was inserted using the pull-through technique, and the position of the bumper was confirmed endoscopically in the body of the stomach. No immediate technical difficulties or postprocedural complications were encountered. His vital signs and complete blood count remained stable before and after the procedure, as shown in Table .
Ten days later, the patient developed bleeding per rectum, which initially was intermittent, bright-red blood mixed with stool. As this was not associated with any instability of his vital signs or change in complete blood count, an elective colonoscopy was requested. However, 48 h later the rectal bleeding became profuse, with passing of large clots. Apart from tachycardia, the blood pressure remained stable, as shown in Table . On examination, the abdomen was soft with normal bowel sounds and no distention or tenderness. A rectal examination revealed fresh red blood with no palpable mass. His hemoglobin level dropped from 13.4 to 9.6 mg/dL, and his white cell count increased to 18.3 × 109/L. Due to ongoing significant rectal bleeding with clots, it was decided to perform an endoscopy, starting with a gastroscopy to rule out an upper gastrointestinal source and then proceeding to colonoscopy.
Upper endoscopy showed no evidence of upper gastrointestinal bleeding, and the PEG tube was noted to be in situ with no evidence of bleeding or any blood until the second part of the duodenum (Fig. ). Colonoscopy showed blood clots in the rectum up to the transverse colon, where a white glistening foreign body was noted. The PEG tube was clearly identified after cleaning and washing to be traversing the transverse colon (Fig. ).
Due to ongoing bleeding, the patient underwent urgent exploratory laparoscopic surgery. The PEG tube was found traversing the anterior abdominal wall and the stomach, with the transverse colon interposed. Segmental transverse colon resection was performed, with removal of the PEG tube and placement of a new one.
Following the operation there was no more rectal bleeding, and the patient tolerated feeding through the PEG tube without any complications.


A 17-year-old girl presented to us with diminished vision since 2 days in her right eye. She had a history of Polycystic ovaries for which she was not taking any medications. Her best-corrected visual acuity (BCVA) was 6/24, N24 in the right eye (OD) and 6/6 in the left eye (OS) on Snellen's chart. Intraocular pressure was 16 and 18 mmHg in OD and OS, respectively. On examination, anterior segment was quiet, and on dilated evaluation, OD showed disc swelling with splinter hemorrhages, and multiple flame-shaped and blot hemorrhages were seen in all quadrants in the retina [Fig. and ] and a normal fundus in OS. Optical Coherence Tomography (OCT) showed neurosensory detachment and cystoid macular edema [].
A diagnosis of CRVO was made and following blood reports were done: complete blood count with erythrocyte sedimentation rate, rheumatoid factor, peripheral smear, lipid profile, antinuclear antibody, urine routine micro, blood sugars, angiotensin converting enzyme, serum homocysteine, blood urea nitrogen, serum osmolality, serum creatinine, D-dimer, and were found to be within normal limits. Chest computed tomography scan [] showed ground glass appearance consistent with COVID-19, but the RT PCR for Covid-19 tested negative in her case.
The patient's mother was COVID-19 positive on RT-PCR and was discharged from the hospital after testing negative a day before the patient presented to us. The patient and the rest of her family had symptoms of cough and fever 21 days before presentation for which they had taken antibiotics, nonsteroidal antiinflammatory agents, and homeopathic medication (Arsenic album). The said symptoms were relieved in 2 days with the medication. The patient was then subjected to Covid-19 Immunoglobulin test, and the test came back positive for IgG against Novel Coronavirus 2019 suggestive of past infection of COVID-19. Based on the above observations, a presumptive diagnosis of CRVO possibly secondary to COVID-19 infection was made. The patient was given intravitreal injection of Ranibizumab 0.05 mL of 10 mg/mL concentration with due precautions. On 1-month follow-up, following the first dose of injection, significant resolution of signs of CRVO was observed and BCVA in OD was 6/18, N10 [ left-side images]. She was advised a second dose of intravitreal anti-VEGF injection, which she received immediately. She came for next follow-up 1 month after the second injection, and her OD fundus showed further resolution of signs of CRVO and macular edema appeared resolved [ right-side images]. Her OD BCVA improved to 6/12, N8. She was advised a third dose of intravitreal anti-VEGF injection and received it at this visit. Her further follow-up after the third injection is due.